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Psychology - Year 1 Forward-approved > PL1030: Biological Psychology > Flashcards

PL1030: Biological Psychology Flashcards

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2
Q

What is the synaptic effect of amphetamine?

A

blocks reuptake of dopamine and other transmitters

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3
Q

What is the synaptic effect of cocaine?

A

blocks reuptake of dopamine and other transmitters

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4
Q

What is the synaptic effect of methylphenidate?

A

gradually blocks dopamine reuptake

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5
Q

What is another name for methylphenidate?

A

Ritalin

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6
Q

What is the synaptic effect of MDMA?

A

releases dopamine and serotonin

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7
Q

What is the synaptic effect of Nicotine?

A

stimulates acetylcholine receptors which among other effects increases dopamine release in the nucleus accumbens

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8
Q

What is the synaptic effect of Opiates?

A

stimulates endorphin receptors

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9
Q

What is the synaptic effect of cannabinoids?

A

triggers negative feedback receptors, which usually respond to anandamide and 2AG on presynaptic cells

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10
Q

What is the synaptic effect of hallucinogens?| like LSD

A

Stimulates serotonin type 2A receptors (5-HT2a)

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11
Q

Where are neurotransmitters and neuropeptides synthesised?

A

transmitters: presynaptic terminalpeptides: cell body

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12
Q

Where are neurotransmitters and neuropeptides released?

A
  • transmitters: axon ending
  • peptides: from dendrites, soma, and sides of axon
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13
Q

Whom are neurotransmitters and neuropeptides released by?

A
  • transmitters: single action potential
  • peptides: repeated depolarisation
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14
Q

What are the effects of neurotransmitters and neuropeptides on their respectively neighbouring cells?

A
  • transmitters: no effect
  • peptides: they also release peptides
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15
Q

How do the effects of neurotransmitters and neuropeptides spread?

A
  • transmitters: to receptors of adjacent postsynaptic cells
  • peptides: diffuse to wide areas
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16
Q

How long do neurotransmitters and neuropeptides effects last?

A
  • transmitters: milliseconds to seconds
  • peptides: minutes
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17
Q

Which five methods can be used to examine the effects of brain damage?

A
  1. study of trauma victims
  2. lesions
  3. ablations
  4. gene knockout
  5. transcranial magnetic stimulation
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18
Q

Which two methods can be used to examine the effects of brain stimulation?

A
  1. stimulating electrodes
  2. optogenetic stimulation
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19
Q

Which six methods can be used to record brain activity while a behaviour is occuing?

A
  1. record from electrodes in the brain
  2. electroencephalograph (EEG)
  3. evoked potentials
  4. magnetoencephalograph (MEG)
  5. positron emission tomography (PET)
  6. functional magnetic resonance imaging (fMRI)
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20
Q

Which two methods can be used to correlate brain anatomy with behaviour?

A
  1. computerised axial tomography (CAT)2. magnetic resonance imaging (MRI)
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21
Q

Records changes in brain activity from the scalp by miliseconds with poor location signal resolution

A

EEG

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22
Q

Records magnetic fields in brain activity from the scalp by miliseconds with poor location signal resolution

A

MEG

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23
Q

Uses radiation to measure brain activity changes over time and location

A

PET

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24
Q

Invasive way of stimulating a brain area, rarely used with humans but frequently with lab animals

A

stimulating electrodes

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25
Q

Records changes in brain activity from the scalp by miliseconds with poor location signal resolution in response to a stimuli

A

evoked potentials

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26
Q

Measures changes in brain activity over around 1 second and identifies locatin within 1 to 2mm

A

fMRI

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27
Q

Uses radiation to map brain areas

A

CAT
| uses X-rays

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28
Q

Maps brain areas in detail using magnetic fields

A

MRI

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29
Q

Invasive way of recording brain activity, rarely used with humans but frequently with lab animals

A

record from electrodesin the brain

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30
Q

Way of examining stimulating effects in any particular type of cell frequently with lab animals

A

optogenetic stimulation

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31
Q

inflicting controlled damage

A

lesion

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32
Q

removing a brain area

A

ablation

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33
Q

intense application of magnetic stimulation to temporarily deactivate a brain area

A

transcranial magnetic stimulation

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34
Q

What is the role of the pretectum in the visual neural pathway?

A

reflex control of pupil and lens

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35
Q

What is the role of the superior colliculus in the visual neural pathway?

A

orienting the movements of headand eyes

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36
Q

What is the role of the hypothalamus in the visual neural pathway?

A

regulates the circadian rhythms

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37
Q

What is the measurement unit for loud sounds?

A

decibels (dB)

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38
Q

Frequency is measured in X and describes….

A

the rate at which sound waves oscillateX= hertz (Hz)

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39
Q

Part of the outer ear are the:

A
  • the pinna
  • auditory canal
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40
Q

Part of the middle ear are the

A
  • ossicles
  • tympanic membrane
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41
Q

Part of the inner ear are

A
  • oval window
  • cochlea
  • auditory vestibular nerve
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42
Q

What is the importance of hair cell depolarization in auditory perception?

A

crucial for the transduction of mechanical stimuli (sound waves) into electrical signals that can be interpreted by the brain, enabling us to hear and perceive sound.

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43
Q

What is the specific neurotransmitter released by hair cells in the cochlea to stimulate sensory neurons?

A

Glutamate

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44
Q

How are the calium and potassium channels in the hair cells connected?

A

The intracellular release of calium during depolarisation also controls the potassium channels

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45
Q

Where is the concentration of rods and cones the highest across the retina?

A
  • Rods in the periphery and in between the fovea and blind spot
  • Cones in the fovea
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46
Q

If you lost all of your cones, which of the following would likely occur?A) Loss of color visionB) Loss of peripheral visionC) Loss of night visionD) Loss of focused perception

A

A and D
| also light sensitivity

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47
Q

What happens if the attentional bottleneck occurs early?

A

Various stimuli compete against each other and only one can pass to be processed further

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48
Q

What happens if the attentional bottleneck occurs later?

A

Various stimuli are subjected to perceptual and semantic analysis after which one stimulus will be selected for aware higher analyis and prompt potential response selection

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49
Q

Which of the following is not a pharmacological treatment for Alzheimer’s disease?
a) Donepezil
b) Memantine
c) Rivastigmine
d) Metformin

A

D

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50
Q

Which class of drugs is commonly prescribed to alleviate symptoms of Alzheimer’s disease?
a) Antidepressants
b) Antipsychotics
c) Cholinesterase inhibitors
d) Anxiolytics

A

C

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51
Q

Which medication is an NMDA receptor antagonist used in the treatment of moderate to severe Alzheimer’s disease?
a) Donepezil
b) Rivastigmine
c) Memantine
d) Galantamine

A

C

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52
Q

What is the primary mechanism of action of cholinesterase inhibitors in Alzheimer’s disease treatment?
a) Blocking glutamate receptors
b) Enhancing cholinergic neurotransmission
c) Inhibiting serotonin reuptake
d) Increasing dopamine levels

A

B

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53
Q

Which of the following drugs is typically prescribed to manage behavioral symptoms such as agitation and aggression in Alzheimer’s patients?
a) Rivastigmine
b) Galantamine
c) Haloperidol
d) Memantine

A

C

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54
Q

What is the primary goal of combining Donepezil and Memantine in the treatment of Alzheimer’s disease?
a) To delay disease progression and improve cognitive function.
b) To reduce behavioral symptoms and agitation.
c) To prevent the formation of amyloid plaques in the brain.
d) To enhance neurogenesis and synaptic plasticity.

A

a

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55
Q
  1. Which stage of Alzheimer’s disease is typically targeted by the combination therapy of Donepezil and Memantine?
    a) Mild cognitive impairment (MCI)
    b) Early-stage Alzheimer’s disease
    c) Moderate to severe Alzheimer’s disease
    d) Advanced dementia
A

C

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56
Q

Lateral inhibition describes

A

the reduced activity in one neuron induced by a neighbouring neuron that is active

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57
Q

Which of the following statements best describes complex cells in the visual cortex?
a) They respond best to stationary stimuli.
b) They respond best to stimuli moving in a specific direction.
c) They are primarily involved in color perception.
d) They are sensitive to changes in brightness.

A

b

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58
Q

Which type of retinal cell is primarily responsible for transmitting visual information from photoreceptors to ganglion cells?a) Bipolar cellb) Complex cellc) Amacrine celld) Horizontal cell

A

a| receives input directly from the receptors

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59
Q

Which type of memory is often associated with skills, habits, and conditioning, and is typically acquired through repetition and practice?a) Declarative memoryb) Non-declarative memoryc) Episodic memoryd) Working memory

A

b

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60
Q

Which type of memory is typically involved in consciously recalling factual information, such as historical dates or personal experiences?a) Declarative memoryb) Non-declarative memoryc) Procedural memoryd) Semantic memory

A

a

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61
Q

What is the primary function of end-stopped cells in visual processing?a) Detection of motionb) Perception of colorc) Recognition of facial featuresd) Detection of line orientation

A

d

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62
Q

How would damage to the striatum affect memory?A. Procedural memory would be affected, one would have odd emotional responsesB. Episodic memory would be affected, one would lose learned skills and habitsC. Procedural memory would be affected, one would lose learned skills and habitsD. Episodic memory would be affected, one would have odd emotional responses

A

C

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63
Q

How would damage to the cerebellum affect memory?A. One would learn odd emotional responsesB. One would lose learned skills and habitsC. One would lose motor coordinationD. One would have odd linguistic responses

A

C| Skeletal musculature

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64
Q

How would damage to the amygdala affect memory?A. One would learn odd emotional responsesB. One would lose learned skills and habitsC. One would lose spatial coordinationD. One would have odd linguistic responses

A

A

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65
Q

Which brain structures are implied in classical conditioning?A. cerebum & amygdalaB. amygdala & hypothalamusC. hypothalamus & cerebellumD. cerebellum & amygdala

A

D

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66
Q

What are three places where damage can lead to auditory degeneration with age?

A
  1. Inner ear2. Auditory nerve3. Brain
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67
Q

Place field cells are most likely to be found in which brain region?a) Hippocampusb) Prefrontal cortexc) Cerebellumd) Amygdala

A

a

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68
Q

Which of the following tasks would most likely be impaired by damage to place field cells?a) Recognizing facesb) Recalling past eventsc) Finding one’s way in a familiar environmentd) Performing mathematical calculations

A

c

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69
Q

What are three common causes of auditory impairments?

A
  1. Pathology of the ossicles.
  2. Obstruction of the auditory canal that blocks the sound wave propagation
  3. Puncturing of the tympanic membrane due to exposure to sudden loud noises.
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70
Q

What does the sympathetic nervous system do

A
  • prepare the organs for a burst of vigorous activity by creating a sympathetic system using the ganglia
  • Prepare the organs for flight, fight or freeze
  • axons release norepinephrine mostly and acetylcholine in minority
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71
Q

How does the sympathetic nervous system prepare the body and its organs for activity?

A

increasing breathing and heart rate and decreasing digestive activity

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72
Q

What activities does the parasympathetic nervous system promote and inhibit, for example?

A
  • increases digestive activity and promotes sexual arousal, including erection in males
  • decreases heart rate
  • conserves energy
  • flow of sinus fluids is a parasympathetic response that releases the neurotransmitter acetylcholine onto the organs
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73
Q

How are the cell body clusters in the parasympathetic system organised?

A
  • Not in interactive chains but long preganglionic axons
  • extend from the spinal cord to parasympathetic ganglia close to each internal organ and short postganglionic fibres extending from the parasympathetic ganglia into the organs themselves
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74
Q

What does the hindbrain consist of and where is it located?

A

The posterior part of the brain consists of the medulla, the pons, and the cerebellum.

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75
Q

What is the brainstem made of

A

the medulla and pons, the midbrain, and certain central structures of the forebrain constitute the brainstem (see Figure 3.8).

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76
Q

Where do cranial nerves originate from and what do they control

A

in the medullavital reflexes such as breathing, heart rate, vomiting, salivation, coughing, and sneezing.

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77
Q

What is the cerebellum known for in terms what it controls

A

many older textbooks describe the cerebellum as important for “balance and coordination” → control of movement
* Types of learning and conditioning, auditory and visual stimuli
* if damaged:trouble shifting their attention back and forth between auditory and visual stimuli

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78
Q

What is the midbrain made of?

A

tectum –> tengmentum (intermediate level of midbrain) –> superior colliculus (visual processing)/ inferior colliculus (auditory processing), substantia nigra (dopamine pathways (movement))

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79
Q

What is the Forebrain and what structure does it include

A

Thalamus, hypothalamus and pituitary gland (next to which we can find the amygdala), basal ganglia

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80
Q

What is the difference between diencephalon and telencephalon

A

thalamus and hypothalamus form the diencephalon, a section distinct from the telencephalon

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81
Q

What is the limbic system

A

interlinked structure under the cerebral cortex forming a border around the brain stem

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82
Q

What is the role of the hypothalamus

A

controlling eating, drinking, temperature control, and reproductive behaviours.

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83
Q

Amygdala

A

evaluating emotional (fear) information

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84
Q

Thalamus

A

sensory processing not olfactory direct to the cortex

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85
Q

What happens to the processed information to what effect

A

transmitted to a single area of the cerebral cortex, as in Figure 3.14. And the cerebral cortex sends information back to the thalamus, prolonging and magnifying certain kinds of input and focusing attention on particular stimuli (Komura et al., 2001).

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86
Q

What are the three germinal layers?*

A
  1. subsections of the ectoderm
    *Surface ecto: nails, hair, skin
    * Neural ecto: neural tube, crest
  2. endoderm –>mucosa of gastro/respiratory system and abdominal organs
  3. mesoderm –>
    * Paraxial: skeleton/muscles;
    * Intermediate: urogenital, kidneys; Lateral plate: limb skeleton, muscular wall
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87
Q

What are the developmental steps of the genesis of the PNS in the first 8 weeks?

A

← form glioblasts (support cells/ Schwann cells), neurons, ependymal cells ← differentiate ventricular layer of spinal chord ← pia mater ← neuroepithelial cells

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88
Q

What are the developmental steps of the genesis of the spinal chord in the first 8 weeks?

A
  • Spinal Chord: neural plate
  • Dorsal root ganglia: ← neural crest cells ← neural ectoderm→ central canal: ventricular layer→
  • grey matter: neuronal bodies ← mantle layer of the neural plate→
  • white matter: axons ← marginal layer*
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89
Q

What is the abreviated neuroembryogenic development?

A

Zygote (linear)/ germ disc (trilaminar meso-ecto-endo) → epiblast cells replace hypoblast → proliferate to form mesoderm → 2nd onwards there is superior lining on the thicked region of the ectoderm notochord due to gastrulation → grows in the direction of the tail (caudal) and induces the notochord formation → ectoderm invaginates (ventral sucilus) → neurolation (folding of the neural plate via notochord induction)

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90
Q

What two categories can cells be placed into

A
  • eukaryotic:membrane-enclosed DNA inside the nucleus ; membrane-bound organelles of varying shapes and sizes
  • prokaryotic: nomembrane-bound DNA and no other membrane-bound organelles
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91
Q

What is the phospholipid bilayer and its railroad track appearance?

A

hydrophobic tails of phospholipids that are the interior of the membrane while their polar head group are seperated by the inner hydrophobic lipid chain portion –> impermeability to hydrophilic molecules, viscosity that allows proteins and phospholipids to move freely

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92
Q

What is cholesterol’s role when it comes to temperature and membrane permeability?

A

can insert itself into the phospholipid bilayer because of its polar hydroxyl group at the end of the phospholipid head group
* High temperature: reduces permeability by hindering the movement of phospholipid of the outer part
* Low temperature: prevents membranes from freezing and maintains membrane fluidity by interfering with interactions between fatty acid chains

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93
Q

What is the fluid mosaic model?

A
  • plasma membrane as a fluid combination of phospholipids, cholesterol, and proteins.
  • Carbohydrates attached to lipids (glycolipids) and to proteins (glycoproteins) extend from the outward-facing surface of the membrane
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94
Q

Which two scientists are regarded as the founders of neuroscience and why?

A

Charles Sherrington: synapse guy
* Santiago Ramón y Cajal: neurons exist as separate units guy

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95
Q

Which type of animal cells do not contain nuclei?

A

Red blood cells

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96
Q

What do the protein channels in the plasma membrane let pass through?

A

controlled flow of water, oxygen, sodium, potassium, calcium, chloride, and other important chemicals

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97
Q

Rough Endoplasmic Reticulum (RER)

A

Membranous network studded with ribosomes involved in protein synthesis

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98
Q

Mitochondria

A

Membrane enclosed organelle responsible for generating chemical energy

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99
Q

Rough Endoplasmic Reticulum (ER)

A

Membranous network involved in lipid synthesis, regulation of calcium and metabolism of carbohydrates

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100
Q

Lysosome

A

Contains enzymes to remove waste

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101
Q

Nucleolus

A

Within the nucleus composed of proteins and nucleic acids

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102
Q

Golgi apparatus

A

Sorts and chemically modifies proteins for specific uses

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103
Q

Cytoskeleton

A

Made up a of different types of tube-like structures responsible for maintaining shape of cell

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104
Q

Smooth Endoplasmic Reticulum (ER)

A

Ribonucleic acids and proteins in the cytoplasm involved in manufacture of proteins

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105
Q

What are ways to study brain-behaviour connection?

A

Investigating Brain Damage
* observing effects of deliberate stimulation TMS

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106
Q

What is optogenetics and why is it used?

A

Research field in which particular cells are stimulated through light
* Psychiatric and medical disorders (narcolepsy) because controlling excitatory and inhibitory functions can be seen/measured

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107
Q

What is an EEG mainly used for?

A

distinguish between wakefulness and sleep stages, if measured repeatedly also for epilepsy; evoked potentials/responses in children that cannot

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108
Q

What’s the benefit of a MEG?

A

Shows temporal changes accurately in 1ms; can identify the amount of time an area responds which forms a wave from point of origin to processing areas

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109
Q

What is a PET device called and how does it measure activity?

A

Cyclotron
* radioactive glucose (a sugar) is injected into a vein
→ PET measures where glucose is used as an indicator of brain activity
→ radioactive atom enhancement decays and releases positron
→ positron collides with neighbouring neurons by sending two gamma rays in the opposite direction
→ PET measures how much radioactive chemicals are in one area from the middle of the two gamma rays

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110
Q

Why are PETs being replaced with fMRIs?

A

expensive , inaccessible and potentially dangerous

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111
Q

What is the difference between fMRI and MRI?

A

MRI records energy released by water molecules after removal of a magnetic field and fMRI does the same for hemoglobin which binds to oxygen whereby hemoglobin with and without oxygen react differently to fMRIs

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112
Q

What are advantages and disadvantages of fMRI?

A
  • Brain activity increases blood flow, aka more haemoglobin to react to, increases oxygen use, so amount of haemoglobin without oxygen decreases → measuring people falling asleep
  • Scans (need more data) + interpretation is difficult (researchers take mean activity, reduce certain areas to their reaction during a task)
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113
Q

What is phrenology and surrounding issues?

A

Inferring brain functions and behaviour form skull

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114
Q

What is a sterotaxic Instrument?

A

Device with an electrode tip which is inserted into a hole in the skull and passes an electrical current in then damaged brain area

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115
Q

What are the different forms of lesions ?

A

Electric - most damaging to axons and neuronsChemical - more common because it either damages, temporarily suspends neurons or synapsesGene-knockout approach - induce a mutation in a gene regulating neural cells, transmitters or receptors

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116
Q

How does transcranial magnetic stimulation work?

A

Magnetic stimulation is applied to the scalp whereby stong stimulation produces a virtual lesion as it deactivates neurons below the magnets –> allows non invasive study of lesions on brain-behaviour link

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117
Q

What are dendrites?

A

branching fibers that get narrower near their ends (etym: tree) that are lined with specialised synaptic receptors that receive information*

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118
Q

What is a cranial nerve?

A

Any peripheral nerve that has its central nervous system connection with the brain, as opposed to the spinal cord.

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119
Q

What’s the difference between vertebrates and invertebrates axons?

A

Vertebrate axons are covered with myelin sheaths interrupted by nodes of Ravier (connected to the spine) while invertebrates do not have that

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120
Q

What is the presynaptic terminal?

A

The end bulb of each dendrite releases chemicals and electrical signals to communicate with other neurons or cells via their postsynaptic bulbs

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121
Q

How do the shape of a neuron and connection relate?

A

Determines function and connective strength more area covered more informational input and output*

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122
Q

What is the ratio of glia and neurons?

A

Glia (etym. Glue of neurons old) outnumber neurons in the cerebral cortex, but neurons outnumber glia in several other brain areas (cerebellum)

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123
Q

Why is A-beta bad?

A

Misfolds and becomes sticky → clumbs to form oligemers → plaquesTrigger the release of cytokines because they’re observed by microglia → neural damage + synapse removal (phagocytosis)

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124
Q

What is the effect of oligimers

A

Weaken synaptic communication → might affect memory

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125
Q

What is neurodegeneration caused by Tau?

A

Tau (components of tangles) usually stablising the cytoskeletal transport → modified → abnormal shape + disconnected from the axon and moves towards the cell body → can spread to healthy neurons spreading tau’s malformation and neurodegeneration

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126
Q

What exactly causes the neural degeneration

A

excessive amounts of Amyloid beta in the cytoplasm of cells, not the external amyloid beta plaques → cytokines activated

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127
Q

Which chromosone has implicated in the production o amyloid beta?

A

21 chromosomes because people with down syndrome also have amyloid beta;

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128
Q

Under which conditions can amyloid-beta reproduce (Eisele et al., 2019)

A

After being boiled, steel still has hints of a-beta that can reproduce; even small scale

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129
Q

What is the amyloid beta hypothesis and related issues?

A

Extracellular a-beta accumulation triggers all pathological processes that culminate in AD → drugs targeting the secretase enzymes are not safe or effective

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130
Q

What is the Tau hypothesis and related issues?

A

Microtubule protein that causes neurodegeneration via breaking down axons and synaptic communication → effective treatments are challenging because of the complex AD pathology

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131
Q

What is the inflammation hypothesis and related issues?

A

Microglia + astrocytes → cytokines: using biomakerker treatments are complicated because they could interfere with the normal immune response

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132
Q

What is the cholinergic and oxidative stress hypothesis and related issues?*

A

Neuronal damage as a result of choline loss which uses acetylcholine → ACh esterase as symptomatic treatment but oxidative stress elevating components cannot be chemically bound to ACh-es

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133
Q

What is are new treatments suggested for AD?

A

Gut microbiome + Immune systemintestinal mucosal lymphoid tissue 70% - 80% of all immune cells in the body + first defence mechanismsCould also directly induce cytokine reaction, via GABA or via enteroendocrine cells that affect the brain through neuroimmune pathwaysCan affect neurotransmitter production and release (vagus nerve)

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134
Q

What is frontotemporal dementia?

A

= pick’s disease → genetic mutation that only causes NFTs and results in degeneration
of the frontal and temporal cortex → emotional changes and loss of executive functions (damaged prefrontal cortex), language disturbance (temporal lobe)

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135
Q

Explain the steps of AD pathogenesis?

A

Amyloid plaques extracellular beta-amyloid + degenerating axons and dendritesactivated microglia and reactive astrocytes, –> neuroinflammatory response produces cytokinesdestroy the degenerating axons and dendrites = only a core of beta-amyloid + neurofibrillary tangles consist of dying neurons that contain intracellular accumulations of twisted filaments of hyperphospholated tau protein –> leaves a trail of deformed and useless axons*

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136
Q

Which enzyme is responsible for what in AD?

A

a gene encodes the production of the ~-amyloid precursor protein (APP), a chain of approx imately 700 amino acids. APP i then cut apmt in two places by enzymes known as secretases to produce AP. TI, e first, P-secretase, cuts the ‘‘tail” off of an APP molecule. The second, y-secretase (gamma-secretase), cuts the “head” off. The result is a molec ule of AP that contains either 40 or 42 amino acids. The location of the second cut of the APP molecule by y-secretase determines which form is produced. In healthy brains, 90-95 percent of the Al3 molecules are of the short form; the other 5-10 percent are of the long form. In patients with Alzheimer’s disease the proportion of long Al3

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137
Q

Which brain region are affected by the neurodegeneration and how does an AD brain look?

A

the hippocampus entorhinal cortexneocortex (especially the association cortex of the frontal and temporal lobes)nucleus basalis locus coeruleus raphe nuclei

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138
Q

What is the other prevalence of AD?

A

10 percent of the population above the age of 6550 percent of people older than 85.

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139
Q

What is the prevalence of lewy bodies?

A

→ earlier framed in the context of parkinson’s now with dementia20% dementia diagnoses

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140
Q

Mild to moderate AD treatments?

A

Cholineesterase inhibitorsImmunotherapies (lecanemab, aducanumab via IV): a-beta in early stage AD slowed rate of cognitive decline vs. reduced a-beta plaques (amyloid-related imaging abnormalities = ARIA)*

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141
Q

Moderate to severe AD treatments?

A

N–methyl-D-aspartate (NMDA) antagonist → later stage regulates glutamate

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142
Q

What are side effects of cholinesterase inhibitors?

A

nausea, vomiting, diarrhea, insomnia, muscle cramps, fatigue, and weight loss., muscle weakness, dizziness

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143
Q

What are side effects of immunotherapeutic drugs?

A

ARIA, , headache, dizziness, falls, diarrhea, and confusion, cough, nausea, vomiting, fever, chills, body aches, fatigue, high blood pressure, low blood pressure, and low oxygen.

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144
Q

What are side effects of N–methyl-D-aspartate antagonistic drugs?

A

dizziness, headache, diarrhea, constipation, and confusion

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145
Q

Whata are side effects of combination treatments?

A

headache, nausea, vomiting, diarrhea, dizziness, anorexia, and ecchymosis (small bruising from leaking blood vessels)

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146
Q

Which medication cannot be taken by AD patients?

A

Sleep aids, anti-anxiety, anticonvulsants, antipsychoti

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147
Q

Which of the following could cause an increase in the amyloid path and, therefore, the formation of plaques?

A

Increased beta-secretase

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148
Q

How many people are affected by Parkinson’s disease?

A

1 to 2 percent of people over age 65 most prevalent movement disorder

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149
Q

What is the pathology of Parkinson’s disease?

A

Increasing loss of dopamine-releasing axons from the substantia nigra to the striatum → striatum decreases inhibition of globus pallidus → globus pallidus increases inhibition to the thalamus→ Damage in substantia nigra <img></img>

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150
Q

What are risk factors and causes of pd?

A

28 genes, toxin exposure, heroin knock-off containing MPTP → MPP+ which accumulates and destroys dopaminergic neurons by disturbing the pathway → mimicking symptoms, insecticides, herbicides, fungicides

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151
Q

What are the symptoms of Parkinson’s disease?

A
  • Muscle tremors
  • Rigidity
  • Slow movements
  • Loss of spontaneous movement (akinesia)
  • Disturbances of posture
  • Depression
  • Dementia
  • Sleep problems
  • Difficulty in smelling
  • Lack of motivation and pleasure
  • Cognitive deficits (attention, memory, language)
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152
Q

When is the onset of Parkinson’s?

A

50s and 60s but symptoms years before

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153
Q

What further complicates the pathology?

A

Imparirment of dopaminergic transmission → more glutamatergic transmission → unbalanced striata (controls output of the basal ganglia) → overactive GABA output

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154
Q

What are lewy bodies?

A

cytoplasmic aggregates that accumulate and contain misfolded and ggregated alpha synuclein proteins

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155
Q

Which treatment might alleviate the symptoms of Parkinson’s?

A

NMDA antagonist if Parkinsons-’s conceptualised as a glutamate hyperactivity disorder?

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156
Q

Which three components have to be shown to lead to Parkinson’s in animal models?

A

6-OHDA → nigral DA neurons think it’s DA → selective destroction of monoaminergic cells → ipsilateral symptomsMPTPSpontaneous genetic mutation → weaver rat DA degeneration over month

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157
Q

What is meant by grafting?

A

Impanting a part of a brain tissueIntracerebral gradting has been shown to be effective for cell replacement → DA release in the sriatum

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158
Q

How did they think that L-dopa can treat Parkinson’s?

A

L-dopa (pre-dopamine) crosses the blood-brain-barrier → increases dopamine release in axons, also deteriorated ones, but not other depleted neurotransmitters; nausea, restlessness, sleep problems, low blood pressure, repetitive movements, and sometimes hallucinations and delusions

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159
Q

What are other ways to treat Parkinson’s?

A
  • Brain tissue transplant? Tough
  • Stem cells? Also complicated
  • Neurotrophins induce via surgery?
  • Inserting electrodes to stimulate the brain: helps interrupt irregular firing
  • Other dopaminergic drugs that haven’t been successful
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160
Q
  1. In what ways is L-dopa treatment disappointing?
A

L-dopa increases dopamine activity in spurts and in all neurons, not steadily and not just in those that need help. It does not stop the loss of neurons.

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161
Q

What procedure has improved the effectiveness of brain grafts for the treatment of Parkinson’s disease?

A

Results improved somewhat after physicians began giving drugs to suppress the immune response.

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162
Q

excitotoxic lesion

A

A brain lesion produced by intracerebra l injection of an excitatory amino acid, such as kainic acid.

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163
Q

stereotaxic surgery (stair ee oh tak sik)

A

Brain surgery using a stereotaxic apparatus to position an electrode or cannula in a specified position of the brain.

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164
Q

bregma

A

The junction of the sagittal and coronal sutures of the skull; often used as a reference point for stereotaxic brain surgery.*

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165
Q

stereotaxic atlas

A

A collection of drawings of sections of the brain ofa particular animal with measurements that provide coordinates for stereotaxic surgery.

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166
Q

fixative

A

A chemical such as formalin; used to prepare and preserve body tissue. formalin (for ma /in) The aqueous solution of formaldehyde gas; the most commonly used tissue fixative.

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167
Q

stereotaxic apparatus

A

A device that permits a surgeon to position an electrode or cannula into a specific part of the brain.

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168
Q

microtome

A

An instrument that produces very thin slices of body tissues.

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169
Q

anterograde labeling method

A

A histological method that labels the axons and terminal buttons of neurons whose cell bodies are located in a particular region.*

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170
Q

immunocytochemical method

A

A histological method that uses radioactive antibodies or antibodies bound with a dye molecule to indicate the presence of particular proteins of peptides.*

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171
Q

retrograde labeling method

A

A histological method that labels cell bodies that give rise to the terminal buttons that form synapses with cells in a particular region.*

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172
Q

transneuronal tracing method.

A

A tracing method that identifies a series of neurons that form serial synaptic connections with each other, either in an anterograde or retrograde direction; involves infection of specific neurons with weakened forms of rabies or herpes viruses*

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173
Q

optogenetic methods

A

The use of a genetically modified virus to insert light-sensitive ion channels into the membrane of particular neurons in the brain; can depolarize or hyperpolarize the neurons when light of the appropriate wavelength is applied.<img></img>*

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174
Q

microelectrode

A

A very fine electrode, generally used to record activity of individual neurons.<img></img>

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175
Q

single-unit recording

A

Recording of the electrical activity of a single neuron.

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176
Q

Give three examples of constructs that can be measured using standardised behavioural tasks in rodents.

A

Forced swim, tail suspension and learned helplessness tests.Tests of anhedonia (for example, sucrose preference, social interaction and sexual behaviour).
* Diverse tests of attention, working memory and episodic memory or prepulse inhibition.

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177
Q

Q: What are behavioural assays used for in animal models of schizophrenia?

A

A: Behavioural assays are used to assess the face validity of animal models of schizophrenia.

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178
Q

What assays might be useful in initial screens?

A

Assays based on acute stress procedures or anxiety-like behaviour might be useful in initial screens, but such screens should not be used as definitive evidence of a depression phenotype. Greater focus on anhedonia and homeostatic symptoms and broadening the scope of these assays would add a useful objective dimension to rodent studies.

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179
Q

Q: Do the transgenic mouse models have construct validity?

A

A: The transgenic mouse models meet some criteria for face and predictive validity, but not construct validity

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180
Q

What is the issue surrounding construct validity and the use of animal research in psychopathology?

A
  1. Injecting animals with a known genetic mutation linked to the disease → not possible
  2. Altering the expression of proteins hypothesised to lead to disease pathogenesis → lack of human evidenceExposure to validated environmental risk factors → not as straightforward
  3. how penetrant a given genetic variant is in producing a disorder/ how clearly linked; lack of human evidence for common genetic variants being irrefutably linked to mental health conditions*
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181
Q

antidepressant that blocks the reuptake of catecholamines and serotonin by presynaptic terminals

A

tricyclic

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182
Q

antidepressant that blocks the reuptake of serotonin in the presynaptic terminal

A

SSRI

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183
Q

antidepressant that blocks the reuptake of serotonin and norepinephrine

A

SNRI

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184
Q

antidepressant that blocks a presynaptic terminal enzyme that metabolizes catecholamines and serotonin into inactive forms

A

MAOI

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185
Q

drug that mimics or increases the effects of a neurotransmitter

A

agonist

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186
Q

affinity

A

tendency of a drug to bind to a receptor

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187
Q

efficacy

A

drug’s tendency to activate the receptor

188
Q

brain area that is rich in dopamine and is central to the brain’s reinforcement system

A

nucleus accumbens

189
Q

craving

A

insistent search for something

190
Q

tolerance

A

decreased effect of a drug after repeated use

191
Q

withdrawal

A

effect of drug cessation

192
Q

antabuse

A

drug that antagonizes the effects of acetaldehyde dehydrogenase by binding to its copper ion

193
Q

methadone

A

drug similar to heroin and morphine that is taken orally

194
Q

SAD

A

seasonal affective disorderdepression that recurs during a particular season, such as winter

195
Q

mania

A

condition characterized by restless activity, excitement, laughter, self-confidence, rambling speech, and loss of inhibitions*

196
Q

lithium

A

element often used as therapy for bipolar disorder

197
Q

presence of behavior not seen in normal people

A

positive symptom

198
Q

negative symptom

A

absence of behavior ordinarily seen in normal people (e.g., lack of emotional expression)

199
Q

concordance

A

similarity, such as having the same disorder as someone else*

200
Q

differential diagnosis*

A

one that rules out other conditions with similar symptoms

201
Q

DISC1 (disrupted in schizophrenia 1)

A

gene that controls production of dendritic spines and generation of new neurons in the hippocampus

202
Q

chemical family that includes antipsychotic drugs that relieve the positive symptoms of schizophrenia*

A

phenothiazinechemical family that includes antipsychotic drugs that relieve the positive symptoms of schizophrenia

203
Q

dopamine hypothesis of schizophrenia

A

idea that schizophrenia results from excess activity at dopamine synapses in certain brain areas

204
Q

movement disorder characterized by tremors and other involuntary movements*

A

tardive dyskinesia

205
Q

second-generation antipsychotic

A

drug that alleviates schizophrenia with less likelihood of movement problems

206
Q

drug that inhibits the NMDA glutamate receptors*

A

phencyclidine (PCP)

207
Q

group of ganglion cell axons that exit through the back of the eye

A

optic nerve

208
Q

area at the back of the retina devoid of receptors

A

blind spot

209
Q

tiny area of the retina specialized for acute, detailed vision

A

fovea

210
Q

opening in the center of the iris where light enters

A

pupil

211
Q

law of specific nerve energies

A

rule that whatever excites a nerve always sends the same information to the brain

212
Q

ganglion cell

A

type of neuron in the retina that receives input from the bipolar cells

213
Q

blind spot

A

area at the back of the retina devoid of receptors

214
Q

neuron in the fovea of humans and other primates*

A

midget ganglion cell

215
Q

chemical contained in rods and cones that release energy when struck by light

A

photopigment

216
Q

horizontal cell

A

type of cell that receives input from receptors and delivers inhibitory input to*

217
Q

thalamic nucleus that receives incoming visual information

A

lateral geniculate nucleus

218
Q

receptive field

A

area in visual space that excites or inhibits any neuron

219
Q

small cell body with small receptive field in or near the fovea

A

parvocellular neuron

220
Q

large cell body with a large receptive field that is distributed evenly throughout the retina

A

magnocellular neuron

221
Q

area responsible for the first stage of visual processing

A

primary visual cortex (area V1)

222
Q

simple cell

A

cell that has a receptive field with fixed excitatory and inhibitory zones

223
Q

blindsight

A

ability to respond in limited ways to visual information without perceiving it consciously

224
Q

hypercomplex cell

A

cell that responds to a bar-shaped pattern of light in a particular orientation

225
Q

strabismus

A

condition in which the eyes do not point in the same direction

226
Q

What are the two types of synapses?

A

Synapses = junctions between neurons allowing communicationelectrical synapses = fast but rarely in the brainchemical synapses: most common in the brain; slow in signalling, but more diverse functions

227
Q

What are neurotransmitters?

A

chemical messengers that allow the transmission of signals across chemical synapses

228
Q

What are the four major structures that compose a neuron?

A

Dendrites, soma (cell body), axon, and presynaptic endings

229
Q

Explain the blood-brain barrier including which cells get to pass

A

viruses> Rabies, spirochete → syphilis Actively transported:

  • Glucose (fuel)amino acids (protein building blocks)
  • Water: through protein channels in the plasma membrane of endothelial cells purines, choline, a few vitamins, iron, hormones and insulin* <img></img>*
230
Q

Why is the blood-brain barrier needed

A

the mechanism that excludes most chemicals from the vertebrate brain is needed because neurons cannot be replaced. When there is an infection there antibodies could potentially distroy neurons like they do in other parts of the body but skin cells or blood cells can be renewed.

231
Q

What cell is crucial for the blood-brain barrier?

A

endothelial cells that form the walls of the capillaries, which do not let viruses nor nutrients pass depending on their ability to dissolve

232
Q

What molecules can pass freely the capillaries of the blood-brain barrier?

A

fat-soluble molecules (vitamins, drugs), small uncharged molecules oxygen & carbon dioxide

233
Q

How do Alzheimer’s and cancer and the blood-brain barrier relate?

A

Capillary walls are weakenedTreatment molecules cannot pass

234
Q

How much glucose and oxygen uses the brain and why?

A

25% of body’s glucose, 20% of oxygen because of energy metabolisation;

235
Q

Why can’t the brain rely on ketone and lactate?

A

glucose is the only nutrient that crosses the blood–brain barrier in large quantities

236
Q

How does the liver produce glucose in case of malnourishment or starvation?

A

from many kinds of carbohydrates and amino acids, as well as from glycerol, a breakdown product from fats but the issue then becomes the lack of vitamin B (thiamine)

237
Q

What does a lack of thiamine lead to?

A

leads to death of neurons and a condition called Korsakoff’s syndrome, marked by severe memory impairments. (common in alcoholism)

238
Q

How much slower would neurons propagate without the myelin sheath?

A

30 times slower

239
Q

What do high concentrations of microglia indicate?

A

Infection, trauma, stroke

240
Q

What are perivascular feet?

A

Astrocytes attach to blood vessels and inducing their endothelial cells to form tight junctions that reinforce the blood-brain barrier and prevent moluclues passing into the cerebral fluid

241
Q

Why do astrocytes absorb potassium ions

A

regulate abnormal accumulation of extracellular potassium ions→ link to epileptic activity

242
Q

How does the electrical gradient function, and what prevents it from collapsing?
What does the sodium-potassium pump do?

A

transports three sodium ions out of the cell while drawing two potassium ions into the cell → sodium 10x outside the cell

243
Q

Why is the electrical and concentration gradient of potassium ions almost equal?

A

Being positively charged, the potassium leak through the membrane even when the gates are shut which increases the electrical gradient

244
Q

How are the electrical and concentration gradients for Potassium and Sodium?

A

Sodium (positive Na+) more concentrated outside but negative electrical gradient to the insidePotassium (K+) more concentrated inside so wants to leave but electrical gradient draws them back → almost balanced

245
Q

What is the function of the resting membrane potential?

A

resting potential prepares the neuron to respond rapidly

246
Q

What are the steps of the action potential?

A

Calcium, sodium channels and potassium channels open → potassium are not girlbosses so nothing happens → sodium channels open so sodium rushes into the axon → positive charge propergates → sodium is me in therapy (shuts down) at the peak of depolarisation but potassium channels stay opened and potassium flows out → depolarised and potassium channels close

247
Q

What are the three principles to remember to understand the chemical basis of the action potential?

A

1.At the start, sodium ions are mostly outside the neuron, and potassium ions are mostly inside.2. When the membrane is depolarized, sodium and potassium channels in the membrane open.3. At the peak of the action potential, the sodium channels close.

248
Q

Q: How does saltatory conduction conserve energy?

A

Saves energy by only letting sodium ions into the nodes of the myelinated part and not at every point of the axon

249
Q

Q: What happens to axons in multiple sclerosis?

A

A: the immune system attacks myelin sheaths → impairments in conducting action potentials and various symptoms including visual impairments and poor muscle coordination.

250
Q

What is the role of inhibitory synapses?

A

Needed for the trade-off between stimulated muscles and the rest
* Sensory input in one part leads to EPSP → to counterbalance

251
Q

What did Sherrington observe about the speed of conduction through reflex arcs, and what did this suggest about the existence of synapses?

A

<15m/s while axon communication is 40m/s
* Interneuronal space communication slows speed down → synapses are responsible<img></img>

252
Q

What is temporal summation, and how did Sherrington use it to explain how repeated stimuli can produce a stronger reflex?

A

Repeated stimuli in short time accumulates → graded potential is created (EPSP/depolarisation) → exceeds the threshold in the postsynaptic neuron if not the excitation decays over time<img></img>

253
Q

What is spatial summation, and how did Sherrington demonstrate this property of synapses?

A

Synaptic input from different locations synchronised (different sensory axons) → EPSP can sum up <img></img>

254
Q

What is the process of synaptic transmission and how does it differ from the conduction of action potentials along an axon?

A

Summation effects vary on the order of sensory input

255
Q

What is the purpose of inhibitory synapses?

A

Inhibitory synapses are a testament of the connections at the spinal chord (when EPSP is triggered in one part an IPSP needs to occur somewhere else) and that muscles counterbalance each other*

256
Q

How do inhibitory synapses work?

A

Postsynaptic cell needs to be hyperpolarised → +potassium channels open and + leaves the cell → or -choloride ions enter the cell*

257
Q

What was Loewi’s experiment and what did he discover?

A

Loewi stimulated a frogs vagus nerve → slows heartbeat and then transferred the fluid around the heart to another frog also slowed heart in second frog → most synapse communicate chemically

258
Q

What are the sequence of events at chemical transmission?

A

Neuron synthesises chemicals
→ neurotransmitters
→ also in axon terminals/ neuropeptides in cell body
→ action potential propagates and calcium releases neurotransmitters in the terminals into the synaptic cleft
→ travel to the postsynaptic neuron
→ neurotransmitter separate from receptors and are potentially returned to presynaptic neuron
→ postsynaptic neuron communicates with presynapse to control neurotransmitters<img></img>

259
Q

What are neurotransmitters and how are they synthesized?

A

Chemicals produced and released by neurons around 100 most shared gaba is the oldest;<img></img>

260
Q

What is MAO, and what is its role in neurons that release serotonin, dopamine, or norepinephrine?

A

Monoamine oxidase enzyme inhibiting the production of neurons that release serotonin, dopamine, or norepinephrine by breaking them into nonfuctioning units → used as basis for antidepressants

261
Q

What is the most common neurotransmitter in the nervous system?

A

Glutamate
* most inhibitory ionotropic synapses function with GABA (gamma-aminobutyric acid), opening chloride gates to have -chloride in the cells
* Glycine mostly in spinal cordAcetycholine mostly excitatory ionotropic synapses

262
Q

What is the difference between ionotropic and metabotropic effects?

A

Sequence of metabolic effects after 30ms not 5ms: smell, pain,taste, arousal, emotion
Don’t depend on GABA or glutamine, but a lot of different NTs
First messenger aka NT binds at receptor → otherside connected with a guanosine triphosphate G-protein releases energy → more second messengers<img></img>

263
Q

What are neuropeptides?

A

Neuromodulators different function to neurotransmitters, similar to hormones in producing longer lasting effects by alterning gene activity

264
Q

What are the six main neurotransmitters found in the brain?

A

Acetylcholine GABA Serotonine Dopamine NorepinephrineEpinephrine

265
Q

The study of humans with brain injuries allowed researchers to find that patients with deficits in speech also presented lesion in_________ area.
a. Amigdala
b. Broca
c. Hippocampus
d. occipital lobe

A

B

266
Q

The main purpose of the Diffusion tensor imaging technique is that it helps researchers identify:
a. which brain regions are particularly active during certain stimuli.
b. how specific brain regions look when they are damaged.
c. white matter and how different brain regions are connected.
d. the timing of brain activity relative to presentation of certain visual stimuli

A

C

267
Q

A researcher wants to compare the volume of grey matter in the brain during development, starting in early development until adulthood. Which of the following methods would be the most suitable?
a. Magnetic resonance imaging (MRI)
b. Computerized tomography (CT)
c. Functional magnetic resonance imaging (fMRI)
d. Optogenetic stimulation

A

A

268
Q

What’s the defining difference between MRI and CT

A

Although CT is used for structural/anatomical imaging of the brain, it requires X-rays - this is not the most suitable to be used in child and multiple times during development.

269
Q

Which of the following statements is MOST true regarding the brains of severely depressed patients?
a. Severely depressed patients’ brains show increased hippocampal volumes as compared to controls.
b. Severely depressed patients’ brains have a lower hippocampal function as compared to healthy individuals.
c. Severely depressed patients’ brains havehigher concentrations of 5-HT and catecholamines.
d. Severely depressed patients’ brains are characterised by up-regulated adult neurogenesis.

A

B

270
Q

Which of the following is a TRUE DISADVANTAGE of Electroconvulsive therapy in depression?
a. It is only used as a supplement to other treatments rather than a therapy by itself.
b. The probability of a quick relapse is high.
c. It takes longer than anti-depressant drugs to provide improvements in the treatment of depression.
d. It is not effective in patients with severe depression.

A

B

271
Q

Which of the following is the MOST accurate regarding the role of the allele polymorphism for the serotonin transporter in depression?
a. Stressful life experiences increase the likelihood of depression in people with the shortgene for the serotonin transporter.
b. People with the long form of the gene for the serotonin transporter have a higher increased probability of depression in response to stressful experiences.
c. People with the short and long forms of the gene for the serotonin transporter have an equal probability of depression in reaction to stressful events.
d. The serotonin transporter is not related to depression.

A

A

272
Q

Which of the following is MOST TRUE regarding the course of the illness for patients with depression?
a. The majority of patients have a long depressive episode and never experience symptoms again.
b. The majority of patients have an episodic illness course and they feel well between acute episodes during their lifetimes.
c. The majority of patients do not recover and experience depression symptoms continuously during their life.
d. The majority of patients have a long depressive episode in their mid-40s.

A

B

273
Q

What is the MAIN mechanism of action of antidepressant drugs?
a. Inhibition of acetylcholinesterase
b. Inhibition of 5-HT and norepinephrine storage in vesicles of presynaptic nerve endings.
c. Blocking serotonin and norepinephrine reuptake transporters.
d. Stimulation of dopamine receptors.

A

C

274
Q

A man has been suffering from severe depression and suicidal ideations after being treated for a year with cognitive-behavioural therapy and multiple antidepressant medication trials. His doctor will now MOST likely prescribe:
a. Monoamine therapy.
b. Electroconvulsive therapy.
c. Psychosurgery
d. Antipsychotic therapy

A

B

275
Q

Which of the following hypotheses BETTER explain the antidepressant drug effectiveness?
a. Antidepressant drugs increase monoamine oxidase activity.
b. Antidepressant drugs lead to increased levels of a neurotrophin (BDNF) important for hippocampal neuronal proliferation and learning.
c. Antidepressant drugs decrease the effects of serotonin and norepinephrine in the brain.
d. Antidepressant drugs lead to neuronal loss and hyperactivity in the right prefrontal cortex

A

B

276
Q

K.S. has been diagnosed with major depression. During her EEG scan, her doctor observes:
a. Hyperactivation of her right prefrontal cortex.
b. Hypoactivation of her right prefrontal cortex.
c. No changes in her prefrontal cortex activation.
d. None of the above.

A

A

277
Q

What does the corpus callosum do?

A

communicate between the two hemispheres

278
Q

What are the layers of the brain/spinal chord? (In order)

A

meningees > dura > arachnoidea > pia

279
Q

Which of the following neurotransmitters aredeactivated by reuptake:
a. Acetylcholine, Ach
b. Dopamine, DA
c. Potassium, K
d. Sodium, NA

A

a

280
Q

What are cones for?

A

daytime lighting, or photopic conditions. 3 types of cones (with different photopigments)<img></img>

281
Q

What are rods?

A
  • nighttime lighting, or scotopic conditions.
  • Higher photopigment concentration.
  • More sensitive to light
  • (with different photopigments)<img></img>
282
Q

Are there rods or cones in the retina?

A

There are no rods in the central fovea, but there are manymore rods than cones in the peripheral retina

283
Q

Explain the process of phototransduction

A

<img></img> In rod cells in the dark, sodium-potassium-pump is in a depolarised state due to cGMP (glutamate release)
–> When light hits rhodopsin channel, it activates transducin
–> activates phosphodiesterase
–> phosphodiesterase breaks down cGMP
–> hyperpolarised cell + decreased glutamate release
–> light stimulus! so rhodopsin is inactivated and via arrestin bound to rhodopsin transducin is blocked
–> cell becomes depolarised + glutamate release until the next light impulse hits

284
Q

What is the reason for color vision deficiency?

A

People with certain genes fail to develop one type of cone,or develop an abnormal type of cone.

285
Q

What’s the prevalence of colour blindness?

A

1 in 12* <img></img>

286
Q

Which gene is responsible for red-green colour deficiency?

A

The gene causing red-green colordeficiency, is on the X chromosome.* <img></img>

287
Q

What are parts of the parallel processing in the visual cortex?

A
  • Ventral stream (towards temporal cortex): identifying and recognizing objects and faces.
  • Dorsal stream (towards parietal cortex): important for identifying where the objects are.
288
Q

What is the IT?

A

<img></img>: inferior temporal cortex recognizes objects –>

289
Q

What’s visual agnosia

A

happens when the inferior temporal cortex is damaged and inhibits object recognition

290
Q

What is the role of the fusiform gyrus

A

recognising faces –> damage: prosopagnosia

291
Q

What is the MT?

A

Area MT: middle temporal cortex (=V5 area) –> responsible for processing visuospatial motion: inability to perceive or detect motion

292
Q

What happens if V4 is damaged?

A

loss of color vision at the corresponding location in the visual field, visual attention and object recognition issues

293
Q

What is the MST?

A

middle superior temporal cortex
* Motion perception
* Damage leads to motion blindness

294
Q

What is the auditory range of humans?

A

0-200db/20-20.000Hz
20-50db for Normal Speech

295
Q

What is the abbreviated pathway of sound to the ear?

A

Sound waves gathered into the outer ear aretransduced from air pressure into mechanicalenergy in the middle-ear ossicles (the hammer,anvil, and stirrup) and into electrochemicalactivity in the inner-ear cochlea.

296
Q

McGurk effect

A

brains give more credit to visual information than to auditory input

297
Q

Rods –

A
  • nighttime lighting, or scotopic conditions. Higherphotopigment concentration. More sensitive to light.
298
Q

vision in the fovea?

A

<img></img>
* daytime lighting, or photopic conditions. 3 types of cones (with different photopigments)<img></img>

299
Q

In retinitis pigmentosa, early symptoms include the loss of peripheral vision and night vision. The loss of what type of cells couldlead to such symptoms?

A

rods

300
Q

What about people with maculardegeneration, which symptoms dothey have?<img></img>

A

cones

301
Q

THE SOUND AND THE EAR ?

A
  • Sound waves gathered into the outer ear aretransduced from air pressure into mechanicalenergy in the middle-ear ossicles (the hammer,anvil, and stirrup) and into electrochemicalactivity in the inner-ear cochlea.
302
Q

Why doesn’t unilateral damage to the inferior colliculus ormedial geniculate nucleus lead to deafness in one ear?

A

sound is split

303
Q

What is the role of the basilar membrane in sound detection?

A

The basilar membrane senses different sound frequencies at specific locations.
* Low-frequency sounds: The membrane vibrates in synchrony with the sound waves.
* The number of firing cells identifies loudness

304
Q

What happens in theTonotopic maps on the basilar membrane and cochlear nucleus?

A

From the base to the apex of the cochlea, the basilar membrane resonates with increasingly lower frequencies. This tonotopy is preserved in the auditory nerve and cochlear nucleus.

305
Q

Why does sound localisation vary?

A

Across three domains:
* Difference in time of arrival
* Difference in intensity between the ears (sound shadow)
* Phase difference between the ears

306
Q

How common are hearing disorders?

A

Hearing loss is the third most common condition among older adults
* 25-40% of people over 65 years old
* 50% of people over 75
* 80% of people over 85

307
Q

What leads to conductive hearing loss

A

Diseases, infections, or tumorous bone growth can prevent the middle ear from transmitting sound waves properly to the cochlea. It includes all pathologies in the external and middle ear.

308
Q

What leads to sensorineural hearing loss

A

Nerve deafness: damage to the cochlea, the hair cells, or the auditory nerve (disease, exposure to loud noises)

309
Q

Presbycusis

A

Age-Related Hearing Loss

310
Q

Age-Related Hearing Loss

A

Degeneration of the sensory cells in the cochlea, supportingcells and auditory nerve; brain areas responsible for languagecomprehension become less active, decreased attentionalcapacities

311
Q

Cochlear implant

A

medical device that uses electricity tostimulate the spiral ganglion cells of the auditory nerve torestore sensorineural hearing loss<img></img>

312
Q

LANGUAGE PERCEPTION

A

Listening to speech activates extensive areas in the temporal lobe, with the activation strongly biased toward the left hemisphere
* Early organization of auditory areas and lateralization for language similar to adults.

313
Q

Developmental changes in native language phonetic perception?

A

Significant increase in performance for the native-language contrast in the first year
* Decline in nonnative perception over the same time period
* <img></img>

314
Q

Selective attention?

A

Difficulty paying attention simultaneouslyto stimuli of the same modality (e.g.,two auditory stimuli or two visual stimuli)

315
Q

Dichotic Listening Task?

A

<img></img>* The simultaneous delivery of different stimuli to the right and the left ears.

316
Q

Cocktail party effect?

A

<img></img>* The cocktail party effect is the selective enhancement of processing resources for a particular target in a noisy environment. Despite high levels of background noise, we can focus on what someone is saying because paying close attention to them enhances our processing of their speech and helps filter out distractors. It works by maintaining the focus of our attention on a single speech source, with extra clues in different sensory modalities, such as the spatial origin of speech sounds, the movements of the speaker’s face, and their unique tone of voice.

317
Q

defining attention

A

cognitive process that allows us toovertlydirect our senses and awareness to specific stimuli due to the frontoparietal and temporoparietal network

318
Q

→ voluntary/ selective attention on stimuli and direction

A

→ enhanced processing, learning

319
Q

→ reflexive attention

A

= involuntarily

320
Q

What are key attentional processes?

A

selection and vigilance

321
Q

How does attention manifest cerebrally?

A

different brain areas and networks are activated across different processes of attention

322
Q

What is the brain activity during attention also linked to?

A

Brain damage

323
Q

What is hemispheral neglect?

A

Damage to one hemisphere of the brain can induce deficits in attention and awareness on the opposite side of the field of vision

324
Q

What is attention, and how is it different from arousal?

A

Attention is the process by which we select or focus on one or more specific stimuli for enhanced processing and analysis. It is the selective quality of attention that distinguishes it from the related concept of arousal, which is the global level of alertness of the individual.

325
Q

Can attention be directed covertly?

A

Yes, attention can be directed covertly. In classic research, Hermann von Helmholtz showed that we can keep our eyes fixed on one location while “secretly” scrutinising some other location in peripheral vision.

326
Q

Q: What is conjunction search?

A

A: Conjunction search is a type of visual search where a person is searching for a target item on the basis of two or more features that together distinguish the target from distracters that may share some of the same attributes. Performance on conjunction searches is directly related to the number of distracters present, and the search involves coordinating multiple cognitive feature maps that overlap with each other, with each map focused on one particular stimulus attribute. This idea is called feature integration theory.

327
Q

Q: What is feature search?

A

A: Feature search is a type of visual search where a person is looking for a target item that is different from all the distractors in some fundamental way. For example, searching for a friend in a red coat in a crowd of dark-suited businesspeople. This type of visual search is known as a feature search because the target feature “pops out” immediately and the search seems effortless.

328
Q

Q: How do voluntary and reflexive attention work together in cognition?

A

A: Voluntary and reflexive attention normally work together in cognition, probably relying on somewhat overlapping neural mechanisms. In single-mindedly searching for specific items (an example of voluntarily controlled attention), a person can be very focused. But even slight noises and movements (cues that reflexively capture attention) can cause a person to stop and scan their surroundings. Effective cues for reflexive attention can cross the boundaries between different sensory modalities in order to aid the processing of stimuli.

329
Q

Q: What are the two important effects seen in experiments using a peripheral spatial cueing task?

A

A: The two important effects seen in such experiments are:
1) a valid cue captures attention and enhances processing of subsequent stimuli in the target location, but only when the interval between cue and target is brief
2) detection of stimuli at the location where the cue occurred is increasingly impaired when the interval between cue and target becomes longer, about 200ms onward. This inhibition of return probably evolved to prevent reflexively controlled attention from settling on unimportant stimuli for more than an instant.

330
Q

Q: What is the function of attention?

A

A: One of the important functions of attention is to act as a filter, blocking unimportant stimuli and directing cognitive resources to only the most important events, and thereby protecting the brain from being overwhelmed by the world.

331
Q

Q: At what level of sensory processing is the attentional bottleneck evident?

A

A: There is debate over whether the attentional bottleneck occurs at an early stage of sensory processing, where unattended information is filtered out right away, or at a later stage where the filtration imposed by the processing bottleneck occurs after substantial analysis has already occurred. Many models of attention contain both early- and late-selection mechanisms, and the debate continues over their relative importance.

332
Q

Q: What is perceptual load and how does it relate to attention?

A

A: Perceptual load is the immediate processing challenge presented by a stimulus. According to the perceptual load theory, when we focus on a complex stimulus that requires a lot of perceptual processing, attention exerts early selection and excludes other stimuli from the outset. But when we focus on simpler stimuli, there is enough perceptual capacity to allow for processing of other stimuli, right up to the level of semantic meaning, recognition, and awareness, and thus, late selection. In other words, attention strikes a balance between early and late selection, according to the difficulty of the task at hand.

333
Q

Q: What is the difference between early and late-selection models of attention?

A

A: Early-selection models propose that unattended information is filtered out right away, at the level of the initial sensory input. Late-selection models, on the other hand, suggest that the filtration imposed by the processing bottleneck occurs at a later point, filtering out stimuli only after substantial analysis has already occurred. Some important but unattended stimuli may undergo substantial unconscious processing right up to the level of semantic meaning and awareness, before suddenly capturing attention. Many models of attention contain both early- and late-selection mechanisms, and the debate continues over their relative importance.

334
Q

Q: What is reflexive attention?

A

A: Reflexive attention, also known as exogenously controlled attention, is the involuntary reorientation of attention toward a sudden or important event, which can capture and draw attention away from the task at hand. It is considered a bottom-up process because it is controlled by sensory inputs from lower levels of the nervous system, rather than being the result of voluntary, conscious cognitive control by the forebrain.

335
Q

Q: How is the effect of reflexive attention on stimulus processing measured?

A

A: The effect of reflexive attention on stimulus processing can be measured using a peripheral spatial cueing task, in which a participant fixates on a point and is asked to respond as quickly as possible when the target stimulus appears. Instead of a meaningful symbol to direct attention toward a target location, a simple task-irrelevant sensory stimulus (such as a flash of light or a sound) is presented in the location to which attention is to be drawn. Reaction time measures for many such trials are averaged for each participant.

336
Q

What is a shadowing task, and how does it relate to attention?

A

A shadowing task is a demanding task in which participants listen to two different streams of dialog delivered simultaneously to the left and right ears, and are asked to focus their attention on one ear or the other and to repeat aloud the material being presented to that ear. Participants can accurately report what they are hearing in the attended ear, but they can report very little that had been presented to the unattended ear. This type of task is used to study selective attention in auditory and visual modalities.

337
Q

What is inattentional blindness, and how can it affect experts?

A

Inattentional blindness is a surprising failure to perceive nonattended stimuli that one would think would be impossible to miss. For example, a gorilla strolling across the screen in a visual shadowing experiment or a clear image of a gorilla inserted into a CT scan of the lungs. It can affect experts as well, with one study showing that 83% of radiologists screening for lung cancer missed the image of a gorilla inserted into a CT scan of the lungs.

338
Q

Inattentional blindness or change blindness

A

The failure to perceive non -attended stimuli that seem so obvious as to be impossible to miss; it was lowering the lights on everything else

339
Q

Function of selective attention?

A

The brain can’t process all sensory information simultaneously

340
Q

What is selective attention?

A

The shifting of our limited selective attentionaround the environment to highlight stimuli forenhanced processing

341
Q

What would it be like if you were equally aware of all the visual and auditory details of your environment at once? Would this be an advantage or a disadvantage?

A

excessive amount of sensory information bombards the brain simultaneously. –> no selective attention no focus/efficiency

342
Q

Overt attention:

A

process in which the personselectively attends to a specific stimulus overothers by moving the eyes to point in thedirection of the stimulus.

343
Q

Covert attention:

A

process that involvesshifting mental attention without moving theeyes.

344
Q

SELECTIVE ATTENTION is an

A

Active process

345
Q

What is a symbolic cuing task and its conclusion and purpose?

A

Study 1: investigate detection ability
Study 1: attention increases our visual sensitivity, making things easier to detect

346
Q

How can you study reaction times? and what is the result of such studies?

A

Study 2: attention speeds reaction times

347
Q

What are top-down processes?

A

endogenousattention: attention is deliberately directedby the brain to some object or place to servea behavioral goal.<img></img>

348
Q

What are bottom-up processes?

A

exogenousattention: the stimulus attracts our attentionwithout any cognitive input. Depends oncertain visual features (e.g., color, movement,novelty,…)<img></img>

349
Q

What do fmris relating human attention to location show?

A

Activated area shifts as the subject changes the area of attention orientation, despite the fact that the stimulus is always the same. Pattern of brain activity changes retinotopically.

350
Q

What do PETs scans relating human attention toshow?

A
  • Task: Frame 1 = Frame 2?
  • Experience of selective attention (shape, colour, speed)and divided attention
  • Increased activity in different brain areas when attention was directed to speed (green), colour (blue) or shape (orange).
351
Q

What do previous studies of neural bases of attention show (3)

A

Visual attention involves activation of the visual cortex and association areas related to the visual system (temporal and parietal lobe).
* The activation of specific areas varies with the characteristics to look for.
* Attention enhances neuronal responses.

352
Q

How is the pulvinar nucleus of the thalamus implicated in attention?

A

Reciprocal connections with visual cortical areas of the temporal, parietal, and occipital lobes. *
* Unilateral injuries to this area lead to increased time responses to stimuli on the contralateral side*

353
Q

How is the frontal eye field (FEF) implicated in atention?

A
  • Area located in the premotor cortex.
  • Responsible for saccades.
  • Direct connections with areas V2, V3, V4 andMT and parietal cortex + superior colliculus<img></img>
354
Q

Which brain region is important for top-down and bottom-up processes

A

<img></img>* Frontal cortex (lateral prefrontal cortex, PFC, and frontal eye fields, FEF) active first during top-down attention, followed by LIP.
* Neurons in the LIP (lateral intraparietal area) responded first to the target during bottom-up attention, followed by the PFC and FEF.

355
Q

What are the two attentional networks?

A

dorsal frontoparietal and right tempoparietal network* <img></img><img></img>

356
Q

How does selective attention influence the gamma frequency in the somatosensory system?

A

increases (important for working memory and attention)

357
Q

SPATIAL NEGLECT

A

People ignore or neglect sensory information located in the visual field opposite the damaged hemisphere. –> More common with lesions of the right hemisphere (the posterior parietal cortex (spatial relations))

358
Q

Why is spatial neglect syndrome a problem in attention but not just sensation?

A

they have difficulty directing their attention to that side. Their brains fail to allocate attentional resources to the neglected space.

359
Q

How many childen are affected byATTENTION-DEFICIT HYPERACTIVITY DISORDER and what are the symptoms?

A
  • Affects around 5% of children
  • inability to sustain attention (inattention): difficulty in staying on a task, staying organized, sustaining focus
  • impulsiveness: acting without thinking or have difficulty with self-control, a desire for immediate rewards
  • hyperactivity: moving constantly, including in situations when it is not appropriate
360
Q

What is proposed to be root of ADHD?

A
  • Delayed cortical development (especiallyin prefrontal regions) in children andadolescentes<img></img>
361
Q

By what are ADHD brains characterised? (3)

A
  1. Cortical thickness (frontal and parietal lobes) is reduced in adults; lower grey matter density; white matter abnormalities* <img></img>*
  2. Reduced total brain volume and/or some brain structures (e.g. amygdala and basal ganglia are smaller)
  3. Involvement of dopamine as well: Levels of available dopamine transporter molecules and receptors are typically lower in some parts of the brain.
362
Q

What is used to treat adhd?

A
  • The most common treatment for ADHD is methylphenidate (Ritalin) – inhibits the reuptake of dopamine and norepinephrine
363
Q

What are the three kinds of learning?

A

Non-associative Learning
1. Habituation
2. Sensitization
Associative Learning
1. Classical Conditioning
2. Operant conditioning
Observational Learning
*Ex: Bandura’s findings in the Bobo doll experiments

364
Q

What is the hebbian synapse?

A

When one cell consistently activates another, the connection between them is strengthened. If it consistently fails to do so, the connection between them is unchanged or weakened* <img></img>

365
Q

What role do synapses play in memory?

A

provides a site for the neuralbasis of learning, a relatively permanentchange in behavior that results fromexperience* <img></img>

366
Q

What does the habitutation of the aplysia show? (initially a gill-withdrawl effect)

A

decreased Ca2+ influx andsubsequently less neurotransmitter release from the presynapticaxon terminal

367
Q

What does the sensitisation of the aplysia suggest? (initially a gill-withdrawl effect)?

A

o increased Ca2+ influx and subsequently moreneurotransmitter release from the presynaptic axon terminal.

368
Q

What would happen to a sensory and motor neuron during non-associative learning

A

more synapses or less

369
Q

What is long-term potention?

A

A long-lasting increase in synaptic effectiveness after high-frequency stimulation

370
Q

Short-term memory

A

storage of information for a limited time

371
Q

Long-term memory

A

storage of of information, that lasts in time – we can recall for days, months, or years after was originally stored

372
Q

Working memory

A

limited in capacity and require rehearsal – information held “in mind” – e.g. when someone tells you his or her phone number, you can retain it for a limited period of time by repeating it

373
Q

Patient H.M. got a bileterall excision of the medialtemporal lobe, including cortex, amygdala, and partof the hippocampus because of epilepsy* <img></img>what would a result look like? if he took a mirror tracing test?

A
  • Severe anterograde amnesia for declarative memory (impairment of long-term memory)
  • Partial retrograde amnesia (loss of episodic/declarative memories)
  • Better implicit than explicit memory (nearly intact procedural memory)
  • Normal working memory
374
Q

The neuronal mechanisms underlying declarative memory, procedural memory or working memory are

A

different

375
Q

Declarative memory (episodic) depends on

A

the medial temporal cortex and hippocampus

376
Q

are important for processing andconsolidating new declarative memories

A

The medial temporal cortex and hippocampus

377
Q

Morris water maze

A

rats with hippocampal lesions do not learn

378
Q

Place Cells:

A

respond selectively only when a mouse is in a certain location in its environment º* <img></img>

379
Q

A rat explores a small box for 10 minutes (left panels). Then the partition is removed, so the rat can explore a larger area (center and right panels).<img></img>explain

A

In this case, an electrode isnext to a cell in the hippocampus that does notrespond when the rat is in the smaller upper box(left). In the first 10 minutes after the partition isremoved, the cell also does not respond (center).But after another 10 minutes, a place field developsin the new larger box (right).

380
Q

Grid cells respond to

A

a series of locations arranged in a hexagonal grid

381
Q

Place cells receive input from…

A

grid cells in the entorhinal cortex

382
Q

Which brain region is important for the implicit memory?

A

the striatum
* Parkinson’s patients (degeneration of neurons in the substantia nigra that project to the striatum) → Difficulty in learning habits
* Patients with Huntington’s disease(degeneration of several areas but in particular the striatum) → Difficulty in learning tasks in which a motor response is associated with a stimulus.

383
Q

Which brain regions deteriorate with AD?

A
  • Severe degeneration of the hippocampus, entorhinalcortex, neocortex (especially the association cortex ofthe frontal and temporal lobes), nucleus basalis, locuscoeruleus, and raphe nuclei* <img></img>
384
Q

Which neurons are among the first to be affected in PD?

A

dopaminergic neurons in substantia nigra- because of Lewy bodies (deposits of alpha-synuclein protein)<img></img>

385
Q

Levodopa chemical decomposition?

A

<img></img>

386
Q

Why is l-dopa often combined with carbi dopa?

A

Carbidopa prevents levodopa from being broken down before it reaches the brain<img></img>

387
Q

Which treatments are used for PD?

A
  • Dopamine agonists
  • MAO inhibitors
  • COMT inhibitors
  • Anticholinergics
  • deep brain stimulation
  • Pluripotent stem cells (PSCs) vs ventral mesencephalon tissue as a cell source for transplantation in Parkinson´s disease
388
Q

What are cognitive and negative symptoms of Schizophrenia?

A
  • poor memory
  • lack of attention
  • reduced decision-making capacity
389
Q

How is Schizophrenia diagnosed?

A

At least two symptoms, being oneof them: delusions, hallucinations, ordisorganized speech. Ongoing for 6 months(at least 1 month of delusions/hallucinations)

390
Q

When is the usual onset of schizophrenia

A

<img></img>

391
Q

What is the risk level for schizophrenia amongst MZs?

A

48%

392
Q

What does schizophrenia affext in the brain?

A

ventricles are enlarged<img></img>

393
Q

Environmental risk factors of schizophrenia?

A

Environmental risk factors:
* Living in cities vs. rural areas
* Childhood trauma
* Autoimmune diseases
* Cannabis use

394
Q

What is the neurodevelopmental hypothesis of schizophrenia?

A

prenatal or neonatal influences produce abnormalities in the developing brain
* Prenatal or childhood infection with the parasite toxoplasma gondii
* Poor nutrition or stress exposure of the mother;season-of-birth effect (winter and early spring)<img></img><img></img>

395
Q

What are the brain abnormalities of schizophrenia and how can they be tracked?

A

pet scan* <img></img>*
* Enlarged ventricles
* Reduced white matter
* Abnormalities in subcortical areas
* Reduced grey matter specially in hippocampus, amygdala, thalamus
* Decreases in brain volume(about 5%)
* Abnormalities visible in blood vessels of the retina
* Dorsolateral prefrontal cortex anatomically affected

396
Q

What is early onset schizophrenia?

A

Comparison of three-dimensionalmaps derived from MRI scans revealsthat, compared with healthy teenagersaged 13 to 18 (left), patients withchildhood-onset schizophrenia (right)have widespread loss of gray matteracross the cerebral hemispheres* <img></img>

397
Q

What are the chemical treatments?

A

*Phenothiazines (e.g., chlorpromazine)
* Butyrophenones (e.g., haloperidol - tradename Haldol)
* These drugs block dopamine type D2synapses

398
Q

Which pathway is responsible for positive symptoms?

A

Mesolimbic pathway| increased DA relese in NAc

399
Q

Which pathway is responsible for negative symptoms?

A

Mesocortical| decresed DA release in prefrontal cortex leads to negative cognitive sym

400
Q

What is the glutamate hypothesis of schizophrenia?

A

schizophrenia results from deficient activity atglutamate synapses in PFC* <img></img>* <img></img>

401
Q

Wht are the class of symptoms of depression?

A

<img></img>* At least five symptoms, being at least oneof them a fundamental one, nearly everyday during a 2-week period. Thesymptoms are clearly different from theindividual´s previous general functioning.

402
Q

Persistent depressive disorder

A

Moderate depression that persists for morethan 2 years (American PsychiatricAssociation, 2013), with at least two of thefollowing symptoms: difficulty with decisionmaking and concentration, feelings ofhopelessness, low appetite or overeating,fatigue, low self-esteem, problems with sleep

403
Q

Which neurochemical systems of depression?

A

<img></img>

404
Q

What is the pathology of depression?

A

results from a deficit of one of theseNT: serotonin and noradrenaline (Monoaminehypothesis)

405
Q

How do stress and depression intersect?

A

elevatedlevels of circulating cortisol –>; failure of negativefeedback mechanisms* <img></img><img></img>of glucocorticoidsalter the serotonin,norepinephrine, and dopaminesignaling systems

406
Q

What happens to the brain in bipolar disorder?

A

gray matter losse anterior insula,prefrontal córtex (ventrolateral,ventromedial, dorsomedia), andsubgenual cingulate cortex.<img></img>

407
Q

What is the inflammatory hypothesis of depression?

A

Cytokines pass the blood brain barrier andstimulate the release of CRH and interactwith noradrenaline, dopamine andserotonin signaling pathways due to infection which influences the BDNF

408
Q

What does the prosencephalon first develop into?

A

The telencephalon and diencephalon

409
Q

What does the mesencephalon develop into in a five-week year old embryo?

A

The midbrain

410
Q

What does the rhombencephalon first develop into?

A

metencephalon and myelencephalon

411
Q

What does the rhombencephalon develop into in a five-week year old embryo?

A

metencephalon (pons & cerebellum) and myelencephalon (medulla oblongata)

412
Q

What does the prosencephalon develop into in a five-week year old embryo?

A

telencephalon (cerebrum) and diencephalon (eye cup, thalamus, hypothalamus)

413
Q
Name the cell components
A

A: Ribosome
B: Rough Endoplasmic Reticulum (RER)
C: Golgi Apparatus
D: Nucleolus
E: Nucleus
F: smooth endoplasmic reticulum (ER)
G: lysosome
H: mitochondria
I: Cell membrane

414
Q

What does this sequence of images show?

A

EEG - TMS machine- PET – FMRI – CT and CT scan – MEG scan

415
Q

Name the hidden parts

A
416
Q

Name the hidden parts of the eye

A
417
Q

Name the hidden parts of the eye

A
418
Q

Which ten structures are part of the visual neural pathway?

A
  1. Eye
  2. Optic nerve
  3. Optic chiasm
  4. Hypothalamus
  5. Optic tract
  6. Pretectum
  7. Superior colliculus
  8. Lateral geniculate nucleus
  9. Optic radiation
  10. Striate cortex
419
Q

What happened if I cut the optic chiasm in the middle?

A

I’d see the right visual hemisfield only with the left eye and the left visual hemisfield only with the right eye

420
Q

The music is really loud it has a
a. high timbre
b. intense frequency
c. complex decibels
d. high amplitude

A

d

421
Q

List the parts of the middle and inner ear

A
422
Q

How is an action potential for a created in the cochlear?

A
  1. Sound waves strike the tympanic membrane
  2. Vibration in the ossicles –> Oval Window
  3. Mechanical pressure waves created in fluid-filled cochlea
  4. Hair cells bend (deflect) along the basilar membrane
  5. Mechanically gated calium and potassium channels open and positive ions flood into the hair cell
  6. Depolarisation of the hair cell releases glutamate triggering post-synaptic sensory neurons
  7. Action potential
423
Q

How invasive are the different neuroimaging techniques?

A
424
Q

What’s the propagation of action potentials?

A
425
Q

What are the features of light?

A
426
Q

What is astigmatism?

A
427
Q

What is presbyopia?

A
428
Q

What is myopia?

A
429
Q

What is hyperopia?

A
430
Q

What are the layers of the fovea?

A
431
Q

What is the trichromatic theory?

A

We perceive colour through the relative rates of response by three kinds of cones, each one maximally sensitive to a different set of wavelengths.

432
Q

Which cone is missing?

A

Image as viewed by an observer lacking green cones (deuteranomaly)

433
Q

Which cone is missing?

A

Image as viewed by an observer lacking blue
cones (tritanopia)

434
Q

Which cone is missing?

A

Image as viewed by an observer lacking red cones (protanopia)

435
Q

What are the odds of inheriting colour deficiency?

A

The gene causing red-green color deficiency, is on the X chromosome.

436
Q

Which visual cortex and other brain regions are implicated in vision?

A
437
Q

How does visual information process from the V1?

A
438
Q

What is the occipital lobe’s, temporal lobe and ventral stream role in vision?

A
439
Q

Transduction by hair cell

A
440
Q

Depolarization of a hair cell

A
441
Q

THE AUDITORY PATHWAY

A
442
Q

How does sound localisation vary?

A
443
Q

What leads to central auditory processing disorders

A
444
Q

What can be said about brain activity in musicians and non-musicians?

A

Nonmusicians showed larger activity on the right than the left hemisphere, whereas musicians showed symmetrical activation

445
Q

What happens during top-down and bottom-up processes in terms of time (voluntary/reflexive)?

A
446
Q

Which brain regions do previous studies of neural bases of attention implicate?

A
447
Q

What is an EPSP and IPSP and how are they caused?

A
  • Excitatory postsynaptic potential (EPSP)
  • Inhibitory postsynaptic potential (IPSP)
448
Q

How does sensory information become memory?

A
449
Q

How does a substantia nigra of a PD patient and a normal person look?

A
450
Q

How does the substantia nigra of a Huntigton’s patient and a normal person look?

A
451
Q

What does this image describe?

A

how the repeated activation of the serotonergic modulatory neurons causes long-term sensitization, requiring new nuclear gene expression and protein synthesis

how something enters into long-term memory

452
Q

What is happening in this picture?

A

Serotonin stimulates a rise in cAMP and activation of PKA in the sensory nerve terminal, causing an increase in the amount of glutamate released when the siphon is touched

something is entering into short-term memory

453
Q

What do these scans of one individual’s brain show?

A

A bipolar brain

454
Q

What would happen?

A
455
Q

What are the symptoms of AD?

A
  • Short-term memory loss
  • Reading problems
  • Pooer object recognition
  • Pooer direction sense
  • Poor judgment
  • Impulsivity
  • Short attention
  • Visual problems
456
Q

Intracranial cannula

A
457
Q

rear surface of the eye, which is lined with visual receptors

A

Retina

458
Q

How can we hear sound?

A
459
Q

explain the neurochemical processes underpinning vision

A
460
Q

What are the synaptic processes that underpin LTP?

A

*glutamate receptors –>
Pre-synaptic neuron → decreased threshold for
producing AP, enhanced release of NT

  • Post-synaptic neuron → increased sensitivity to NT
    (more AMPA receptors) + increased kinases which prompt the insertion of AMPA in the postsynaptic spine –> more sensitive to glutamate
    –> repeated so Mg2 is driven out of postsynaptic NDMA receptors
461
Q

What are the four important principles of observational learning?

A
462
Q

Explain

A rat explores a small box for 10 minutes (left
panels). Then the partition is removed, so the rat
can explore a larger area (centre and right panels).

A

Color coding indicates the area in the box where
one place cell in the hippocampus responds: red,
large response; yellow, moderate response; blue, no
response. This cell has a place field in the smaller
upper box; when the partition is removed, it stays in
the same location

463
Q

When is the usual onset of schizophrenia

A
464
Q

Which neurochemical systems of depression?

A

Psychology - Year 1 Forward-approved (4 decks)

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