PL1030: Biological Psychology Flashcards
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What is the synaptic effect of amphetamine?
blocks reuptake of dopamine and other transmitters
What is the synaptic effect of cocaine?
blocks reuptake of dopamine and other transmitters
What is the synaptic effect of methylphenidate?
gradually blocks dopamine reuptake
What is another name for methylphenidate?
Ritalin
What is the synaptic effect of MDMA?
releases dopamine and serotonin
What is the synaptic effect of Nicotine?
stimulates acetylcholine receptors which among other effects increases dopamine release in the nucleus accumbens
What is the synaptic effect of Opiates?
stimulates endorphin receptors
What is the synaptic effect of cannabinoids?
triggers negative feedback receptors, which usually respond to anandamide and 2AG on presynaptic cells
What is the synaptic effect of hallucinogens?| like LSD
Stimulates serotonin type 2A receptors (5-HT2a)
Where are neurotransmitters and neuropeptides synthesised?
transmitters: presynaptic terminalpeptides: cell body
Where are neurotransmitters and neuropeptides released?
- transmitters: axon ending
- peptides: from dendrites, soma, and sides of axon
Whom are neurotransmitters and neuropeptides released by?
- transmitters: single action potential
- peptides: repeated depolarisation
What are the effects of neurotransmitters and neuropeptides on their respectively neighbouring cells?
- transmitters: no effect
- peptides: they also release peptides
How do the effects of neurotransmitters and neuropeptides spread?
- transmitters: to receptors of adjacent postsynaptic cells
- peptides: diffuse to wide areas
How long do neurotransmitters and neuropeptides effects last?
- transmitters: milliseconds to seconds
- peptides: minutes
Which five methods can be used to examine the effects of brain damage?
- study of trauma victims
- lesions
- ablations
- gene knockout
- transcranial magnetic stimulation
Which two methods can be used to examine the effects of brain stimulation?
- stimulating electrodes
- optogenetic stimulation
Which six methods can be used to record brain activity while a behaviour is occuing?
- record from electrodes in the brain
- electroencephalograph (EEG)
- evoked potentials
- magnetoencephalograph (MEG)
- positron emission tomography (PET)
- functional magnetic resonance imaging (fMRI)
Which two methods can be used to correlate brain anatomy with behaviour?
- computerised axial tomography (CAT)2. magnetic resonance imaging (MRI)
Records changes in brain activity from the scalp by miliseconds with poor location signal resolution
EEG
Records magnetic fields in brain activity from the scalp by miliseconds with poor location signal resolution
MEG
Uses radiation to measure brain activity changes over time and location
PET
Invasive way of stimulating a brain area, rarely used with humans but frequently with lab animals
stimulating electrodes
Records changes in brain activity from the scalp by miliseconds with poor location signal resolution in response to a stimuli
evoked potentials
Measures changes in brain activity over around 1 second and identifies locatin within 1 to 2mm
fMRI
Uses radiation to map brain areas
CAT
| uses X-rays
Maps brain areas in detail using magnetic fields
MRI
Invasive way of recording brain activity, rarely used with humans but frequently with lab animals
record from electrodesin the brain
Way of examining stimulating effects in any particular type of cell frequently with lab animals
optogenetic stimulation
inflicting controlled damage
lesion
removing a brain area
ablation
intense application of magnetic stimulation to temporarily deactivate a brain area
transcranial magnetic stimulation
What is the role of the pretectum in the visual neural pathway?
reflex control of pupil and lens
What is the role of the superior colliculus in the visual neural pathway?
orienting the movements of headand eyes
What is the role of the hypothalamus in the visual neural pathway?
regulates the circadian rhythms
What is the measurement unit for loud sounds?
decibels (dB)
Frequency is measured in X and describes….
the rate at which sound waves oscillateX= hertz (Hz)
Part of the outer ear are the:
- the pinna
- auditory canal
Part of the middle ear are the
- ossicles
- tympanic membrane
Part of the inner ear are
- oval window
- cochlea
- auditory vestibular nerve
What is the importance of hair cell depolarization in auditory perception?
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.
What is the specific neurotransmitter released by hair cells in the cochlea to stimulate sensory neurons?
Glutamate
How are the calium and potassium channels in the hair cells connected?
The intracellular release of calium during depolarisation also controls the potassium channels
Where is the concentration of rods and cones the highest across the retina?
- Rods in the periphery and in between the fovea and blind spot
- Cones in the fovea
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 and D
| also light sensitivity
What happens if the attentional bottleneck occurs early?
Various stimuli compete against each other and only one can pass to be processed further
What happens if the attentional bottleneck occurs later?
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
Which of the following is not a pharmacological treatment for Alzheimer’s disease?
a) Donepezil
b) Memantine
c) Rivastigmine
d) Metformin
D
Which class of drugs is commonly prescribed to alleviate symptoms of Alzheimer’s disease?
a) Antidepressants
b) Antipsychotics
c) Cholinesterase inhibitors
d) Anxiolytics
C
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
C
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
B
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
C
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
- 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
C
Lateral inhibition describes
the reduced activity in one neuron induced by a neighbouring neuron that is active
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.
b
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| receives input directly from the receptors
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
b
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
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
d
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
C
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
C| Skeletal musculature
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
Which brain structures are implied in classical conditioning?A. cerebum & amygdalaB. amygdala & hypothalamusC. hypothalamus & cerebellumD. cerebellum & amygdala
D
What are three places where damage can lead to auditory degeneration with age?
- Inner ear2. Auditory nerve3. Brain
Place field cells are most likely to be found in which brain region?a) Hippocampusb) Prefrontal cortexc) Cerebellumd) Amygdala
a
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
c
What are three common causes of auditory impairments?
- Pathology of the ossicles.
- Obstruction of the auditory canal that blocks the sound wave propagation
- Puncturing of the tympanic membrane due to exposure to sudden loud noises.
What does the sympathetic nervous system do
- 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
How does the sympathetic nervous system prepare the body and its organs for activity?
increasing breathing and heart rate and decreasing digestive activity
What activities does the parasympathetic nervous system promote and inhibit, for example?
- 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
How are the cell body clusters in the parasympathetic system organised?
- 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
What does the hindbrain consist of and where is it located?
The posterior part of the brain consists of the medulla, the pons, and the cerebellum.
What is the brainstem made of
the medulla and pons, the midbrain, and certain central structures of the forebrain constitute the brainstem (see Figure 3.8).
Where do cranial nerves originate from and what do they control
in the medullavital reflexes such as breathing, heart rate, vomiting, salivation, coughing, and sneezing.
What is the cerebellum known for in terms what it controls
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
What is the midbrain made of?
tectum –> tengmentum (intermediate level of midbrain) –> superior colliculus (visual processing)/ inferior colliculus (auditory processing), substantia nigra (dopamine pathways (movement))
What is the Forebrain and what structure does it include
Thalamus, hypothalamus and pituitary gland (next to which we can find the amygdala), basal ganglia
What is the difference between diencephalon and telencephalon
thalamus and hypothalamus form the diencephalon, a section distinct from the telencephalon
What is the limbic system
interlinked structure under the cerebral cortex forming a border around the brain stem
What is the role of the hypothalamus
controlling eating, drinking, temperature control, and reproductive behaviours.
Amygdala
evaluating emotional (fear) information
Thalamus
sensory processing not olfactory direct to the cortex
What happens to the processed information to what effect
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).
What are the three germinal layers?*
- subsections of the ectoderm
*Surface ecto: nails, hair, skin
* Neural ecto: neural tube, crest - endoderm –>mucosa of gastro/respiratory system and abdominal organs
- mesoderm –>
* Paraxial: skeleton/muscles;
* Intermediate: urogenital, kidneys; Lateral plate: limb skeleton, muscular wall
What are the developmental steps of the genesis of the PNS in the first 8 weeks?
← form glioblasts (support cells/ Schwann cells), neurons, ependymal cells ← differentiate ventricular layer of spinal chord ← pia mater ← neuroepithelial cells
What are the developmental steps of the genesis of the spinal chord in the first 8 weeks?
- 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*
What is the abreviated neuroembryogenic development?
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)
What two categories can cells be placed into
- 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
What is the phospholipid bilayer and its railroad track appearance?
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
What is cholesterol’s role when it comes to temperature and membrane permeability?
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
What is the fluid mosaic model?
- 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
Which two scientists are regarded as the founders of neuroscience and why?
Charles Sherrington: synapse guy
* Santiago Ramón y Cajal: neurons exist as separate units guy
Which type of animal cells do not contain nuclei?
Red blood cells
What do the protein channels in the plasma membrane let pass through?
controlled flow of water, oxygen, sodium, potassium, calcium, chloride, and other important chemicals
Rough Endoplasmic Reticulum (RER)
Membranous network studded with ribosomes involved in protein synthesis
Mitochondria
Membrane enclosed organelle responsible for generating chemical energy
Rough Endoplasmic Reticulum (ER)
Membranous network involved in lipid synthesis, regulation of calcium and metabolism of carbohydrates
Lysosome
Contains enzymes to remove waste
Nucleolus
Within the nucleus composed of proteins and nucleic acids
Golgi apparatus
Sorts and chemically modifies proteins for specific uses
Cytoskeleton
Made up a of different types of tube-like structures responsible for maintaining shape of cell
Smooth Endoplasmic Reticulum (ER)
Ribonucleic acids and proteins in the cytoplasm involved in manufacture of proteins
What are ways to study brain-behaviour connection?
Investigating Brain Damage
* observing effects of deliberate stimulation TMS
What is optogenetics and why is it used?
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
What is an EEG mainly used for?
distinguish between wakefulness and sleep stages, if measured repeatedly also for epilepsy; evoked potentials/responses in children that cannot
What’s the benefit of a MEG?
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
What is a PET device called and how does it measure activity?
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
Why are PETs being replaced with fMRIs?
expensive , inaccessible and potentially dangerous
What is the difference between fMRI and MRI?
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
What are advantages and disadvantages of fMRI?
- 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)
What is phrenology and surrounding issues?
Inferring brain functions and behaviour form skull
What is a sterotaxic Instrument?
Device with an electrode tip which is inserted into a hole in the skull and passes an electrical current in then damaged brain area
What are the different forms of lesions ?
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
How does transcranial magnetic stimulation work?
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
What are dendrites?
branching fibers that get narrower near their ends (etym: tree) that are lined with specialised synaptic receptors that receive information*
What is a cranial nerve?
Any peripheral nerve that has its central nervous system connection with the brain, as opposed to the spinal cord.
What’s the difference between vertebrates and invertebrates axons?
Vertebrate axons are covered with myelin sheaths interrupted by nodes of Ravier (connected to the spine) while invertebrates do not have that
What is the presynaptic terminal?
The end bulb of each dendrite releases chemicals and electrical signals to communicate with other neurons or cells via their postsynaptic bulbs
How do the shape of a neuron and connection relate?
Determines function and connective strength more area covered more informational input and output*
What is the ratio of glia and neurons?
Glia (etym. Glue of neurons old) outnumber neurons in the cerebral cortex, but neurons outnumber glia in several other brain areas (cerebellum)
Why is A-beta bad?
Misfolds and becomes sticky → clumbs to form oligemers → plaquesTrigger the release of cytokines because they’re observed by microglia → neural damage + synapse removal (phagocytosis)
What is the effect of oligimers
Weaken synaptic communication → might affect memory
What is neurodegeneration caused by Tau?
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
What exactly causes the neural degeneration
excessive amounts of Amyloid beta in the cytoplasm of cells, not the external amyloid beta plaques → cytokines activated
Which chromosone has implicated in the production o amyloid beta?
21 chromosomes because people with down syndrome also have amyloid beta;
Under which conditions can amyloid-beta reproduce (Eisele et al., 2019)
After being boiled, steel still has hints of a-beta that can reproduce; even small scale
What is the amyloid beta hypothesis and related issues?
Extracellular a-beta accumulation triggers all pathological processes that culminate in AD → drugs targeting the secretase enzymes are not safe or effective
What is the Tau hypothesis and related issues?
Microtubule protein that causes neurodegeneration via breaking down axons and synaptic communication → effective treatments are challenging because of the complex AD pathology
What is the inflammation hypothesis and related issues?
Microglia + astrocytes → cytokines: using biomakerker treatments are complicated because they could interfere with the normal immune response
What is the cholinergic and oxidative stress hypothesis and related issues?*
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
What is are new treatments suggested for AD?
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)
What is frontotemporal dementia?
= 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)
Explain the steps of AD pathogenesis?
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*
Which enzyme is responsible for what in AD?
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
Which brain region are affected by the neurodegeneration and how does an AD brain look?
the hippocampus entorhinal cortexneocortex (especially the association cortex of the frontal and temporal lobes)nucleus basalis locus coeruleus raphe nuclei
What is the other prevalence of AD?
10 percent of the population above the age of 6550 percent of people older than 85.
What is the prevalence of lewy bodies?
→ earlier framed in the context of parkinson’s now with dementia20% dementia diagnoses
Mild to moderate AD treatments?
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)*
Moderate to severe AD treatments?
N–methyl-D-aspartate (NMDA) antagonist → later stage regulates glutamate
What are side effects of cholinesterase inhibitors?
nausea, vomiting, diarrhea, insomnia, muscle cramps, fatigue, and weight loss., muscle weakness, dizziness
What are side effects of immunotherapeutic drugs?
ARIA, , headache, dizziness, falls, diarrhea, and confusion, cough, nausea, vomiting, fever, chills, body aches, fatigue, high blood pressure, low blood pressure, and low oxygen.
What are side effects of N–methyl-D-aspartate antagonistic drugs?
dizziness, headache, diarrhea, constipation, and confusion
Whata are side effects of combination treatments?
headache, nausea, vomiting, diarrhea, dizziness, anorexia, and ecchymosis (small bruising from leaking blood vessels)
Which medication cannot be taken by AD patients?
Sleep aids, anti-anxiety, anticonvulsants, antipsychoti
Which of the following could cause an increase in the amyloid path and, therefore, the formation of plaques?
Increased beta-secretase
How many people are affected by Parkinson’s disease?
1 to 2 percent of people over age 65 most prevalent movement disorder
What is the pathology of Parkinson’s disease?
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>
What are risk factors and causes of pd?
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
What are the symptoms of Parkinson’s disease?
- 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)
When is the onset of Parkinson’s?
50s and 60s but symptoms years before
What further complicates the pathology?
Imparirment of dopaminergic transmission → more glutamatergic transmission → unbalanced striata (controls output of the basal ganglia) → overactive GABA output
What are lewy bodies?
cytoplasmic aggregates that accumulate and contain misfolded and ggregated alpha synuclein proteins
Which treatment might alleviate the symptoms of Parkinson’s?
NMDA antagonist if Parkinsons-’s conceptualised as a glutamate hyperactivity disorder?
Which three components have to be shown to lead to Parkinson’s in animal models?
6-OHDA → nigral DA neurons think it’s DA → selective destroction of monoaminergic cells → ipsilateral symptomsMPTPSpontaneous genetic mutation → weaver rat DA degeneration over month
What is meant by grafting?
Impanting a part of a brain tissueIntracerebral gradting has been shown to be effective for cell replacement → DA release in the sriatum
How did they think that L-dopa can treat Parkinson’s?
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
What are other ways to treat Parkinson’s?
- 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
- In what ways is L-dopa treatment disappointing?
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.
What procedure has improved the effectiveness of brain grafts for the treatment of Parkinson’s disease?
Results improved somewhat after physicians began giving drugs to suppress the immune response.
excitotoxic lesion
A brain lesion produced by intracerebra l injection of an excitatory amino acid, such as kainic acid.
stereotaxic surgery (stair ee oh tak sik)
Brain surgery using a stereotaxic apparatus to position an electrode or cannula in a specified position of the brain.
bregma
The junction of the sagittal and coronal sutures of the skull; often used as a reference point for stereotaxic brain surgery.*
stereotaxic atlas
A collection of drawings of sections of the brain ofa particular animal with measurements that provide coordinates for stereotaxic surgery.
fixative
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.
stereotaxic apparatus
A device that permits a surgeon to position an electrode or cannula into a specific part of the brain.
microtome
An instrument that produces very thin slices of body tissues.
anterograde labeling method
A histological method that labels the axons and terminal buttons of neurons whose cell bodies are located in a particular region.*
immunocytochemical method
A histological method that uses radioactive antibodies or antibodies bound with a dye molecule to indicate the presence of particular proteins of peptides.*
retrograde labeling method
A histological method that labels cell bodies that give rise to the terminal buttons that form synapses with cells in a particular region.*
transneuronal tracing method.
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*
optogenetic methods
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>*
microelectrode
A very fine electrode, generally used to record activity of individual neurons.<img></img>
single-unit recording
Recording of the electrical activity of a single neuron.
Give three examples of constructs that can be measured using standardised behavioural tasks in rodents.
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.
Q: What are behavioural assays used for in animal models of schizophrenia?
A: Behavioural assays are used to assess the face validity of animal models of schizophrenia.
What assays might be useful in initial screens?
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.
Q: Do the transgenic mouse models have construct validity?
A: The transgenic mouse models meet some criteria for face and predictive validity, but not construct validity
What is the issue surrounding construct validity and the use of animal research in psychopathology?
- Injecting animals with a known genetic mutation linked to the disease → not possible
- Altering the expression of proteins hypothesised to lead to disease pathogenesis → lack of human evidenceExposure to validated environmental risk factors → not as straightforward
- 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*
antidepressant that blocks the reuptake of catecholamines and serotonin by presynaptic terminals
tricyclic
antidepressant that blocks the reuptake of serotonin in the presynaptic terminal
SSRI
antidepressant that blocks the reuptake of serotonin and norepinephrine
SNRI
antidepressant that blocks a presynaptic terminal enzyme that metabolizes catecholamines and serotonin into inactive forms
MAOI
drug that mimics or increases the effects of a neurotransmitter
agonist
affinity
tendency of a drug to bind to a receptor
What happens in theTonotopic maps on the basilar membrane and cochlear nucleus?
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.
SELECTIVE ATTENTION is an
Active process
What is a symbolic cuing task and its conclusion and purpose?
Study 1: investigate detection ability
Study 1: attention increases our visual sensitivity, making things easier to detect
How can you study reaction times? and what is the result of such studies?
Study 2: attention speeds reaction times
What do fmris relating human attention to location show?
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.
What do PETs scans relating human attention toshow?
- 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).
How is the pulvinar nucleus of the thalamus implicated in attention?
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*
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
What does this sequence of images show?
EEG - TMS machine- PET – FMRI – CT and CT scan – MEG scan
Name the hidden parts
Name the hidden parts of the eye
Name the hidden parts of the eye
Which ten structures are part of the visual neural pathway?
- Eye
- Optic nerve
- Optic chiasm
- Hypothalamus
- Optic tract
- Pretectum
- Superior colliculus
- Lateral geniculate nucleus
- Optic radiation
- Striate cortex
What happened if I cut the optic chiasm in the middle?
I’d see the right visual hemisfield only with the left eye and the left visual hemisfield only with the right eye
The music is really loud it has a
a. high timbre
b. intense frequency
c. complex decibels
d. high amplitude
d
List the parts of the middle and inner ear
How is an action potential for a created in the cochlear?
- Sound waves strike the tympanic membrane
- Vibration in the ossicles –> Oval Window
- Mechanical pressure waves created in fluid-filled cochlea
- Hair cells bend (deflect) along the basilar membrane
- Mechanically gated calium and potassium channels open and positive ions flood into the hair cell
- Depolarisation of the hair cell releases glutamate triggering post-synaptic sensory neurons
- Action potential
How invasive are the different neuroimaging techniques?
What’s the propagation of action potentials?
What are the features of light?
What is astigmatism?
What is presbyopia?
What is myopia?
What is hyperopia?
What are the layers of the fovea?
What is the trichromatic theory?
We perceive colour through the relative rates of response by three kinds of cones, each one maximally sensitive to a different set of wavelengths.
Which cone is missing?
Image as viewed by an observer lacking green cones (deuteranomaly)
Which cone is missing?
Image as viewed by an observer lacking blue
cones (tritanopia)
Which cone is missing?
Image as viewed by an observer lacking red cones (protanopia)
What are the odds of inheriting colour deficiency?
The gene causing red-green color deficiency, is on the X chromosome.
Which visual cortex and other brain regions are implicated in vision?
How does visual information process from the V1?
What is the occipital lobe’s, temporal lobe and ventral stream role in vision?
Transduction by hair cell
Depolarization of a hair cell
THE AUDITORY PATHWAY
How does sound localisation vary?
What leads to central auditory processing disorders
What can be said about brain activity in musicians and non-musicians?
Nonmusicians showed larger activity on the right than the left hemisphere, whereas musicians showed symmetrical activation
What happens during top-down and bottom-up processes in terms of time (voluntary/reflexive)?
Which brain regions do previous studies of neural bases of attention implicate?
What is an EPSP and IPSP and how are they caused?
- Excitatory postsynaptic potential (EPSP)
- Inhibitory postsynaptic potential (IPSP)
How does sensory information become memory?
How does a substantia nigra of a PD patient and a normal person look?
How does the substantia nigra of a Huntigton’s patient and a normal person look?
What does this image describe?
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
What is happening in this picture?
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
What do these scans of one individual’s brain show?
A bipolar brain
What would happen?
What are the symptoms of AD?
- Short-term memory loss
- Reading problems
- Pooer object recognition
- Pooer direction sense
- Poor judgment
- Impulsivity
- Short attention
- Visual problems
Intracranial cannula
How can we hear sound?
explain the neurochemical processes underpinning vision
What are the synaptic processes that underpin LTP?
*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
What are the four important principles of observational learning?
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).
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
When is the usual onset of schizophrenia
Which neurochemical systems of depression?
