Biopsychology Flashcards

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1
Q

How does the brain send messages to the body?

A
  • Through the nervous system (rapid/costly, network structure determines what cells receive
  • Through vascular system (slow/cheap, membrane receptors determine what cells receive
  • Think cost benefit trade off
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2
Q

Describe the history of life

A
  • Prokaryotic cell (bacteria)
  • Eukaryotic cell (more specialised cell that has more functions)
  • Metazoa (first animals, multi cellular, digestive chamber
  • Bilateria (digestive tract with separate front and mouth, muscle present)
  • Chordates (tail for movement, beginnings of spinal chord)
  • Vertebrates
  • Jawed fish
  • Mammals
  • Primates
  • Homo
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3
Q

What are the key points of evolution across species?

A
  • Brain areas have associated function
  • Humans and vertebrates share a similar gross structure
  • Size of relative brain area indicates functional specialisation
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4
Q

How does an FMRI scanner work?

A
  • When neurons become active, blood flows to the part of the brain to provide oxygen to fuel the cells.
  • Hemoglobin (the iron-containing oxygen transporting protein present in blood) differs in how it responds to magnetic fields, depending on whether it has a bound oxygen molecule
  • The MRI scanner, which is basically a giant magnet, detects these small changes in the magnetic field.
  • not directly measuring brain activation. We are measuring blood flow (more precisely, the magnetic properties of oxygenated vs deoxygenated blood)
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5
Q

What are the problems with a bold signal?

A

-Arbitrary, slow (4-5 second delay), 16 seconds to return to baseline

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6
Q

What is a block design in relation to FMRI scans?

A

-long periods of alternating task/baseline performance (task/rest/task/rest ect)

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7
Q

What are the weaknesses of block designs?

A
  • Highly predictable occurrence of stimuli: subjects know what is coming and may alter strategies accordingly (not always a pro)
  • Inflexible for more complex tasks
  • Ecological validity. Does blocking trials change the psychological process
  • Can’t separate trials by performance – e.g. to look at activation associated with correct vs incorrect response
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8
Q

What is an event related design?

A

-Trials of different conditions are randomly intermixed and occur close together in time

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9
Q

What are the advantages of even-related designs?

A
  • Flexible and can be randomised to eliminate practice effects and predictability
  • Post hoc sorting of responses from conditions
  • Can look at novelty and priming (rare/unpredictable events)
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10
Q

How is data collected from an FMRI?

A
  • Volume of slices is collected (2-3 secs)

- Brain areas are referenced through universal mapping using voxels (3x3x3 mm cube referenced as a coordinate)

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11
Q

How is data processed from an FMRI scan?

A
  • High pass filter (remove low frequency oscillations such as scanner drift)
  • Motion correction
  • Slice time correction (time between slices being gathered)
  • Coregistration (spatial alignment of several images)
  • Normalisation (spatial transformation of brains into a common space, making them comparable to each other. Uses a universally recognised “average brain”
  • Spatial smoothing (modelling of neurons that may fire around a neuron that has fired)
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12
Q

How is data from an FMRI scan analysed?

A
  • Bold signal correlated with time course of each condition
  • T-Test btween values from each condition (seen as differing colour on scan)
  • Adjust P value to account for error (130,000 voxels x 0.05 degree of certainty means false positives will be found)
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13
Q

What are the two types of data analysis used in this research and their strengths and weaknesses?

A
  • Whole brain analysis (+ whole brain used, no hypoth needed/- loose spatial resolution, “laundry list of areas” that meaningless and difficult to interpret)
  • Region of interest analysis (+hypoth driven no laundry list, simpler analysis, lends itself to meta analysis/- easy to miss other things going on in the brain, not always easy to define regions)
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14
Q

What are the overall limitations of FMRI?

A
  • Correlative

- Low temporal resolution (accuracy in relation to time)

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15
Q

What is the corpus callosum?

A

-White matter tracts that connect the two brain hemispheres

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16
Q

What is the cerebal cortex?

A

-Grey matter on the outer part of the brain (nerve cell neurons, dendrites)

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17
Q

Where is white matter situated?

A

-Under the grey matter of the brain (long elongated axons)

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18
Q

What is a gyrus and a sulcus?

A
  • Gyrus is the plateau on the cortical surface

- Sulcus is the ditch or fold on cortical surface (major ones can be referred to as fissures)

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19
Q

Describe the four lobes and how they’re separated

A
  • Lobes : frontal, parietal lobe, temporal lobe, occipital lobe
  • Central sulcus (vertical split from frontal & parietal lobe)/ Lateral fissure (horizontal split from temporal to frontal and parietal lobes)/ Parieto-occipital sulcus (occipital lobe from temporal & parietal lobes)
  • The frontal lobe is important for cognitive functions and control of voluntary movement or activity. The parietal lobe processes information about temperature, taste, touch and movement, while the occipital lobe is primarily responsible for vision. The temporal lobe processes memories, integrating them with sensations of taste, sound, sight and touch.
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20
Q

What terms describe brain orientations?

A
  • Superior/Dorsal refers to surface of the brain, Inferior/Ventral refers to structures within the brain
  • Anterior/Rostral refers to front of the brain (forehead), Posterior/Caudal refers to back of the brain (back of the head)
  • Medial refers to structures in the middle of the brain (between hemispheres), Lateral refers to structure in left or right hemisphere
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21
Q

What are the different images of slicing referred to as?

A
  • Axial slice (horizontal slices from top to bottom)
  • Coronal slice (vertical slice from front to back)
  • Sagittal slice (vertical from left to right)
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22
Q

Name three spefic groups of neurons and their functions

A
  • The reticular formation, a complex network of cells in the core of the brainstem involved in the control of arousal and sleep.
  • The suprachiasmatic nucleus (Hypothalamus) controls the circadian (24 hr) biological rhythms
  • The ventromedial nucleus (Hypothalamus) controls the conversion of blood glucose into body fat
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23
Q

Describe the process of perception

A
  • The cortical areas where the sensory information arrives (via relay nuclei in the brainstem, particularly via the Thalamus) are referred to as primary visual/auditory/sensory-motor areas
  • This perceptual information then gets passed to the secondary sensory areas, where more sophisticated processing takes place
  • From the secondary sensory areas, the processing moves to the association areas, where information from different modalities and of different types is integrated
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24
Q

Describe the process of motor control

A
  • The primary motor cortex exerts direct control over movement
  • However, other areas (premotor and supplementary motor) are involved in the planning of movement and integration of motor behaviour with other behaviour
  • In addition, some sub-cortical structures (Basal Ganglia) and brainstem structures and groups of cells (Cerebellum; Substantia Nigra) are also involved in the fine-grained co-ordination and timing of movements
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25
Q

Describe a non-essential activation

A
  • Some process A essential for the task may often co-occur with another process B that is not essential for the task
  • For instance, reading on a computer/laptop often goes hand in hand with typing on it, so a task of reading on a computer screen may elicit activations related to typing but typing is unlikely to be causally related to reading performance
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26
Q

What is neuropsychology?

A

-Neuropsychology is the area of psychology that examines the effects of brain damage on abilities and behaviour.

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27
Q

What are the key approaches to neuropsychology?

A
  • Classical neuropsychology (primarily focuses on localisation)
  • Cognitive neuropsychology (focused on cognitive architecture/equipotentialilaty/dissociation’s)
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28
Q

What is a single dissociation and its weakness?

A
  • Analysing psyhcological processes without knowing the exact location of the damage
  • However, at close scrutiny this single dissociation is not sufficient for drawing a conclusion
  • For instance, it is possible that the same mental computations are used for both, but suppose that consonant letters are easier to differentiate visually from each other than vowel letters
  • This could make consonants more resilient to the effects of brain damage, but would not necessarily demonstrate a qualitative difference in the way they are processed (read and written)
  • But - if consonants are generally more resilient to the effects of brain damage, one should not find any patients with impaired processing of consonants and relatively spared processing of vowels
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29
Q

What is a double dissociation?

A

-The existence of such opposite patterns is referred to as double dissociation

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30
Q

What are the strengths and weaknesses of neuropsychology?

A
  • advantage of neuropsychology over electrophysiology and neuroimaging is that it enables causal inference
  • The main drawback is that lesions resulting from trauma or neurological degeneration are rarely anatomically selective- they tend to affect multiple brain regions/structures
  • Also, brain damage is always associated with general cognitive, emotional and personality changes whose effect on cognitive performance is very considerable and difficult to separate from the effects of damage to a specific region/structure
  • Ethically can’t recreate damage
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31
Q

What is TMS?

A

-Transcranial magnetic stimulation
A large current is briefly discharged into a coil of wire held on the subject’s head.

  • The current generates a rapidly changing (increasing) magnetic field around the coil of wire and this field passes into the brain.
  • In the cortex, the magnetic field generates electric (ionic) current through neurons’ membranes
  • Can stimulate motor cortex (muscle contractions occur) & visual cortices (flashing patterns known as phosphenes)
  • Referred to as a virtual lesion as the activation often causes disorganisation of neural activity causing an effect similar to that of a lesion
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32
Q

What are the advantages/disadvantages of TMS?

A
  • Strengths: Can determine causation
  • Good spatial resolution and excellent temporal resolution
  • Is reversible allows for within group analysis and is ethical
  • Weaknesses: Can’t be used as a control due to noise and sensation it elicits
  • Can’t reach deeper brain regions
  • More subtle than actual brain damage
  • Can elicit seizures especially in those with epilepsy (is considered safe)
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33
Q

Describe what a micro-electrode recording is

A
  • Electrical activity can be measured from brain tissue using very thin electrodes (micro-electrodes) inserted into the tissue
  • The technique is also referred to as single-cell recordings, because typically the data are acquired from single brain cells (neurons)
  • Because these recordings are invasive (one needs to perform surgery to do them), they are performed in humans only when they undergo brain surgery
  • What is typically measured is the firing rate (or spike rate)- the frequency of action potentials a cell generates
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34
Q

What is a strength and weakness of micro-electrode recordings?

A
  • Strength: most precise and direct measure of brain activity
  • Weakness: Highly invasive (restricted in both subjects and brain areas)
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35
Q

What does EEG stand for?

A

-Electroencephalography

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36
Q

What is field potential?

A
  • A temporary deficit of positive charge develops in the area of extracellular space where sodium enters the neuron
  • A temporary surplus of positive charge develops in the area near the soma, where potassium exits the cell
  • This creates field potential outside of the neuron
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37
Q

How is an EEG different from micro-electrode recordings?

A
  • EEG can’t detect spiking behaviour (action potential) as they can’t reflect the electrical fields elicited and action potentials are to small/short
  • Also are less sensitive to brain structures located deeper within the brain
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38
Q

Give strengths and weaknesses of EEG’s/ERP’s

A
  • Strength: Cheaper and more portable than other methods (fMRI)/ high temporal resolution
  • Weakness: Can lack precision as multiple frequencies can be in-bedded in a recording as EEG measures a more general area than single-electrode recordings/ limited spatial resolution
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39
Q

What is an ERP?

A
  • Methodological analysis of EEG, by extracting time-locked specific events from raw EEG data
  • Background activity is removed stimulus is shown multiple times to create an average signal
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40
Q

What are the CNS and PNS? and their overall purpose?

A
  • CNS= central nervous system (brain and spinal chord)
  • PNS= peripheral nervous system (everywhere else in the body)
  • Monitor and regulate inner organs , release chemicals, change internal states (sleep,hunger,emotions)/ Analyse info from the body and environment/ generate responses & motor control
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41
Q

What are the neuron zones?

A
  • Input zone (soma, dendrites) neurons collect and integrate information
  • Integration zone (between soma & axon) decision to produce signal is made
  • Conduction zone (axon) where information can be transmitted over distances
  • Output zone (axon terminals) where neuron transfers information to other cells
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42
Q

How does a neuronal membrane allow transmission from inside and outside of cell

A

-Selectively permeable membrane allows transmission via channels (have to be specific size & charge)

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43
Q

How do ions move across cell membranes?

A
  • Diffusion (high to low gradient) occurs when ion channel is open
  • Electrostatic forces (opposites attract, like charges repel)
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44
Q

Describe the accumulation of ions at a cell membrane?

A
  • Ion distribution differs inside and outside of cell which forms an electrochemical gradient (due to electrostatic forces)
  • Neural cell membrane accumulates charges on both sides acting as capacitor (similar to a battery)
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45
Q

Describe what happens when neuronal membrane is in a semipermeable state?

A

-Ions start to move being pushed or pulled back depending how the electrochemical gradient changes as ions cross the membrane.

For example:

Diffusion through leak channel allows K+ out of the cell, but then there is slightly more positive charge outside, and slightly more negative charge inside. So electrostatic forces rapidly start to pull K+ back in …

Diffusion through voltage-gated Na+channels of Na+ into the cell along the concentration gradient, but the more enters the more positive becomes the intracellular cytoplasm. So electrostatic forces start pushing Na+ back out if the channels do not close or unless equal amounts of K+ flow out at the same time (for example through leak and open voltage-gated K+ channels)

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46
Q

Identify and explain what the three classes of ion channels are?

A
  • Gated ion channels remain closed until activation for a very brief period of time, either by electrical signals (voltage-gated) or by drugs or messenger molecules (ligand-gated).
  • Ion pumps actively transport ions in and out of the neuron
  • Leak channels allow a specific ion type to freely diffuse (e.g. they are always open and let K+ through but not Na+)
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47
Q

How do ion pumps work? What are the most important?

A
  • Capture small molecules (e.g. Na+, K+ or Ca2+) from one side of the membrane and carry them across to the other side against concentration gradient.
  • Powered through temporary phosphorylation of pump’s catalytic subunit which breaks off one phosphate group of ATP, synthesised by mitochondria, which becomes ADP After some time. The phosphate group is uncoupled to free up the binding site for the next transport action.
  • Na/K pump (three Na out and 2 K in)
  • Ca pump (takes Ca out of cytoplasm)
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48
Q

What is a leak channel and how does it work?

A

-Potassium channels in the cell membrane that are always open and allow only potassium to pass through

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49
Q

What are microelectrode recordings?

A

-Neuronal signals are measured as difference in potentials on each side of the membrane (units – Volt) by creating an electrical circuit that connects wired electrodes with the fluids of the neural tissue

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50
Q

What is resting potential in a neuron?

A

-membrane potential of a nerve cell at rest, e.g. neuronal membrane is polarised (typically -70 mV, inside of axon is negatively charged)

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51
Q

What is a neural signal

A

-change of resting potential to more negative or positive potential when ions move across the membrane

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52
Q

Describe what a graded potential/action potential is and what is meant by hyperpolarisation/depolarisation

A
  • Hyper= more negative than resting potential
  • Depolar= more positive than resting potential
  • Graded= a potential that can either be hypo or depol
  • Action= Always depol that creates a response greater than the neuron specific threshold, greater excitation over the threshold creates greater frequency of actio potentials (size of action potential always stays the same)
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53
Q

Describe an action potential

A
  • Resting potential – voltage-gated channels are closed
  • Rising phase – shooting up in the depolarisation caused by the opening of voltage-gated Na+ ion channels
  • Overshoot – the membrane potential becomes positive as more and more Na+ flow into the cell (positive feedback loop)
  • Falling phase – Na+ ion channels become inactivated and close, while K+ channels open leading to a reduction of positive charge inside of the cell
  • Undershoot – K+ ion flow out of the cell through the open K+ channels
  • Recovery - refractory period during which all channels are closed and membrane potential returns to resting value
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54
Q

Name three types of synapses

A

-Axo dendritic, axo somatic and axo axonic

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55
Q

Describe ionotropic receptors interaction in post synaptic transmission

A
  • Action potential opens Ca channels, Ca triggers vesicle fusion and neurotransmitter release, neurotransmitter binds with ionotropic receptors opening ion channels
  • This is a fast signal transmission
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56
Q

What are ligandgated ion channels and autoreceptors?

A
  • Channels that opened when bound with neurotransmitters

- Communicate to presynaptic cells the net concentration of neurotransmitter in the cleft

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57
Q

Describe how a metabotropic receptor works

A
  • Neurotransmitter binds to G protein coupled receptor
  • G protein is activated
  • G protein travels to adjacent ion channel (brief delay)
  • Opens ion channel
  • This is a slow, long lasting varied process
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58
Q

What is a non-spiking neuron?

A

A neuron that doesn’t generate action potentials, have no on/off switch and are more sensitive to signal noise

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59
Q

What helps to compensate for signal loss in neuron transmission?

A
  • Thciker axons better insulate signal
  • Nodes of ravier work as myelin insulation offers considerable resistance to the flow of ionic currents across the membrane, the action potential jumps from node to node. This process is called saltatory conduction
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60
Q

Describe excitatory synapses and inhibitory synapses

A
  • Action potential in excitatory synapse causes depolarisation in postsynaptic neuron (causes it to fire)
  • Action potential in inhibitory synapse causes hyperpolarisation in postsynaptic neuron (doesn’t fire)
  • The sum of these signals at a neuron determines the outcome (e.g. if two excitory responses and one inhibitory response are received by a neuron the sum of the three together determine the response)
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61
Q

How is information coded in neural networks?

A
  • In feedforward circuits the signal is distributed to many neurons through divergence of their connections, or is determined by collecting signals from from many neurons through convergence.
  • ) Spatial and temporal summation at the synapses determine the strength of the signal when it is passed on from one neuron to the next
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62
Q

How do feedback loops work?

A
  • Feedback loops (positive, negative) provide direct or indirect input influencing signals and thus information
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63
Q

How does training increases synpase efficiency?

A
  • Increased release of neurotransmitter
  • Increased membrane size or sensitivity
  • Pre and post synaptic size
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64
Q

Describe two forms of synaptic plasticity

A
  • Preysnaptic depression where continued exposure to a stimulus causes habituation and a weaker response. This is because less neurotransmitter is released over time and eventually retraction of some synaptic terminals (sea hare)
  • Sensitisation where inter-neuron modulation (neuron gives more neurotransmitter to another neuron) increases strength of response. As seen sea hare which was shocked before given stimulus increasing strength of response. Is an example of non-associative learning
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65
Q

How has the hippocampus been shown to be involved in memory?

A
  • Maquire found taxi drivers have larger hippocampi for spatial learning and route memory
  • Morris found that rats with lesions over their hippocampi had their memory impaired
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66
Q

What does LTP stand for?

A

-First discovered by Terje Lømo in 1966, long-term potentiation (LTP) is a long-lasting strengthening of synapses between nerve cells due to continued strong firing. Psychologists use LTP to explain long-term memories.

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67
Q

How do AMPA/NMDA receptors work?

A
  • AMPA receptors are ionotropic receptors that open when glutamate binds to them allowing Na to pass through them into postsynaptic neuron causes a excitatory response
  • NMDA are both ligand and voltage gated, they are blocked by a Mg plug. Open if glutamate binds to them and membrane depolarises (Because of AMPA receptors) to expel Mg plug. This leads to an influx in Ca and creates EPSP and LTP (EPSP stands for excitatory response)
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68
Q

How do AMPA and NMDA receptors help LTM?

A

-AMPA activating NMDA allows for Ca to activate CREB that then targets genes responsible for growing new dendritic spines and synapses

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69
Q

What evidence is there that shows NMDA receptors are important in spatial learning?

A

Morris gave rats AP5 treatment which inhibited NMDA receptors (blocks them). The rats could not learn spatial learning task

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70
Q

Describe synaptic transmission of Ca

A
  • When the action potential reaches the axon terminal, it opens Ca2+ voltage-gated channels
  • Ca2+ has higher concentration outside, hence the concentration gradient pushes it into the cell
  • Ca2+ ions have a specific property: they interact with neurotrasmitter vesicles (storage), pushing them towards the membrane
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71
Q

Describe synaptic transmission

A
  • Once the vesicles containing the neurotransmitter reach the membrane, they open up and the neurotransmitter is released into the “synaptic cleft”
  • The neurotransmitter then binds to its receptors in the postsynaptic neuron. If these receptors are themselves ion-channels, they open when the neurotransmitter interacts with them
  • If the receptors are not ion channels, they interact with specific ion channels and eventually open them
  • As a consequence, ions enter the postsynaptic neuron, resulting in a Post-Synaptic Potential
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72
Q

What is inactivation and recycling of neurotransmitter?

A
  • Inactivation= Diffusion: the transmitter is “lost” in the inter-cellular space & Enzymatic degradation: enzymes break down the transmitter
  • Recycling = re-uptake where the transmitter is recycled either in the pre-synaptic or the post-synaptic neuron. This is the most economical way to inactivate the transmitter
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73
Q

Name four ways drugs can influence the synaptic sequence with an example

A
  • propagation of the action potential e.g. TTX is toxin, found in some fish, that block ion channels in nodes of ravier in the respiratory system leading to death (paralyses muscles)
  • the release of the transmitter e.g. tetanospasmin toxin interferes with GABA vesicles and binds to cell membrane, instead of vesicle, reducing amount of GABA released. Leads to muscle contractions as GABA inhibits this/ aphetamines in contrast effect dopaminergic pathways (increases dopamine) such as VTA linked to reward
  • modulate how the transmitter interacts with the post-synaptic channels (receptors) e.g. curare acts as a ANTAGONIST (blocks but does not activate a channel) in acetylcholines receptors in excitatory synapses causing paralysis/ Heroin is an AGONIST (imitates behaviour of a neurotransmitter increasing its effect) of endorphines which bind to opiate receptors reducing muscle pain and inducing relaxation
  • modulating its inactivation and recycling e.g. cocaine blocks the transporter of dopamine and nor-adrenaline preventing re-uptake and boosting their effect.
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74
Q

What is a monoamine?

A

-Neurotransmitter with a single amino group such as dopamine, adrenaline, serotonin and melatonin

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75
Q

Describe how two psychoactive substances work

A
  • Caffeine= Many of the neurons that release substances like dopamine and adrenaline (catecholamines) also release a self-inhibiting transmitter- adenosine. Adenosine binds to its receptors in the pre-synaptic neuron and inhibits the release of catecholamines. Caffeine competes with adenosine for its receptors (it is an antagonist), blocking adenosine and thus reducing its inhibitory effect. It also inhibits cAMP which regulates energy levels in cells thus increasing glucose metabolism in them
  • Alcohol= agonist of GABA so induces relaxation and in higher doses binds to GABA channels leading to sedation. Indirectly stimulates dopamine releases leading to small euphoria.
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76
Q

Describe psychoactive substances are used to treat psychiatric conditions

A

-Benzodiazepines (valium) are used to treat anxiety disorders. Anxiety disorders are characterised by deficits in GABA, valium act as agonists of GABA. They are non-competitive and bind to other sites than what GABA binds to
-MAO inhibitors prevent MAO enzyme from breaking down serotonin, dopamine and noradrenaline, used to treat depression
/ SSRIs inhibits transporter and re uptake of serotonin

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77
Q

Describe the neuropatholofy of cocaine

A
  • Cocaine addiction is associated with a number of brain damage risks appearing minutes to hours after cocaine consumption, including stroke in young adults in their early thirties, seizures, lesions resulting in movement disorders
  • More subtle pathology includes reduced volume of the inferior portion of the frontal lobe
78
Q

Describe the neuropathology of heroin

A

reduction in grey matter, brain hypoxia (reduced oxygen availability), cerebral edema (water saturation), stroke (loss of blood supply), spongiform leukoencephalopathy (general loss of brain white matter - axons) and myelopathy (paralysis produced by spinal lesions).

79
Q

Describe the neuropathology of alcohol

A

-Alcoholism is strongly linked to the Wernicke–Korsakoff syndrome characterized by anterograde amnesia (inability to remember new things),

80
Q

Describe the neuropathology of cannabis

A
  • Brain volume reduced in users in the hippocampus and the amygdala.
  • indicating a doubling of the risk of psychotic symptoms (such as those found schizophrenia) given because of heavy cannabis use
81
Q

What is the estimate of how much genetics contribute to addiction?

A
  • 50%
82
Q

What are the four causal factors associated with addiction? with an example

A
  • Effects of drug-related cues – cue reactivity e.g. associating an addiction with cues such as smoking with friends. These cues create a conditioned response that can contribute to relapse
  • Effects of drug tolerance and withdrawal e.g. conditioned compensatory response is a response given by the body to help counter the effects of drugs to avoid harmful consequences it acts as a from of tolerance (reducing heart rate when taking cocaine) however this response can happen because of cues with the substance not needing to be present (syringe, people, room). Siegel (1982) rat study. Withdraw symptoms are caused by this effect, the body trying to compensate for a substance that is no longer present.
  • The drugs’ influence on processing of rewards (pleasure and incentives (motivation) e.g. anhedonia hypothesis states that dopaminergic pathways responsible for pleasure and this causes addiciton this is contradicted by the incentive salience hypothesis that states drugs influence the dopaminergic circuit to influence motivation to obtain the drug (euphoria does also contribute) creating long term addiction
  • Drug taking as self-medication in mental illness e.g. to alleviate symptoms, casual link between the two each could be responsible for each other
83
Q

Describe the hierarchy of the motor control system

A

-Premotor/supplementary motor cortex/ parietal cortex (actions and planning) > primary motor cortex > brainstem > spinal cord (output)

84
Q

How does the spinal chord communicate movement?

A

-Action potential in motor neurons in the spine releases acetylcholine (causes muscle fibers to contract) the frequency of these action potentials and number of muscle fibers determine the force the muscle generates

85
Q

Describe two subcortical motor structures in the brain stem

A
  • Cranial nerves responsible for reflexes (eating, breathing, facial expressions)
  • Extrapyramidal tracts (posture, movement speed)
86
Q

Describe two subcortical motor structure outiside of the brainstem

A
  • Cerebellum (balance and body coordination)

- basal ganglia (imitations of actions)

87
Q

Describe the primary motor cortex

A
-Receives input from almost all cortical motor regions, Crossed hemispheric, control
Somatotopic organisation (different areas for different parts of the body)
88
Q

What areas are associated with cortical motor regions?

A

-parietal and prefrontal cortex (involved in representation of space and attention)

89
Q

How do neurons encode movement?

A
  • Encode end point (not trajectory, monkeys study)
  • Encode direction of movement (monkey study) vector is direction neuron prefers, population vector is the summed preferred direction of individual neurons
90
Q

How does the motor system adapt and how has this been shown?

A
  • Cerebellum is important for learning new mapping known as forward models (make predictions) and primary motor cortext is important for consolidating this
  • tDCS stimulates these areas with an electric current applied to the scalp, participants with this adapted faster
  • TMS experiments using cerebellum found that interference of this area impeded the accuracy of prediction
91
Q

Describe the basal ganglias role in motor control

A

-Helps balance excitatory and inhibitory activation that balances movement (loss of neurons in this area can result in a tremor or slowed movement)

92
Q

What is the first stage in processing sensory information?

A
  • Receptor neurons such as photo receptors in the eye respond to stimulus
  • Receptors neurons then communicate this to CNS system directly (touch) or through exciting sensory neurons (sound) different brain areas are responsible for different senses
  • Some animals have sensory neurons adapted for additional sense such as echolocation in bats
93
Q

What is serial processing?

A

-Process of signal being communicated from receptor to associating cortex (not hierarchical)

94
Q

What are mechanoreceptors?

A

-Different touch receptors (vibration, pain, touch) with distinct pathways to the brain to allow different qualities of the skin to be communicated individually

95
Q

What are the main receptors found in human skin, their function and size of their receptive field

A

-Meissner’s corpuscles (touch)/(S), Merkel’s discs (touch)/(S), Ruffini’s endings (stretch)/(L), free nerve endings (pain/temperature)/(S), Pacinian corpuscle (vibrationan & pressure)/(L)

96
Q

What is a receptive field?

A

-The space in which a stimulus can affect a neurons firing rate

97
Q

How does the pacinian corpuscle work?

A

-Vibration or pressure deforms corpuscle and stretches the tip of axon opening mechanically gated ion channels

98
Q

What are cell thresholds?

A
  • The strength of a stimulus needed to vary the response of a cell
  • Cells with overlapping fields can therefore respond differently due to their thresholds allowing different stimulus’s to be detected
99
Q

How can thresholds change over time

A

-Receptors can adapt their thresholds, if the prevailing range of stimulus intensities changes, to optimise coding of the stimulus e.g. light receptors when going from a dark to a light room

100
Q

What are phasic and tonic receptors?

A
  • Phasic = receptors that show fast loss of response to a stimulus (Meissner’s and Pacinian corpuscle)
  • Tonic = receptors that adapt slowly to a stimulus (Merkels disc and Ruffini’s ending)
101
Q

How does the brain know where different sensory inputs are coming from and ?

A

-Somatotopic mapping where body regions are adjacent to regions in the cortex

102
Q

How can sensory inputs be suppressed?

A
  • Accessory organ such as eyelid or muscles in ear

- Top down process e.g. brain stem sends messages to receptor cells in the ear to selectively dampen sounds

103
Q

How can cortical maps be reorganised?

A

-Experience-dependent plastic reorganisation (e.g. after training or loss of a body part)

104
Q

What is vision?

A

-Detecting and interpreting patterns

of electromagnetic radiation

105
Q

What receptor cells are located on the retina and how are they different ?

A

-Cones used to see colour and require more light and rods which work in low levels of light

106
Q

What receptor cells are located on the retina and how are they different ?

A

-Cones used to see colour and require more light so are used during the day and rods which work in low levels of light

107
Q

How does light pass through the eye and how does it compensate for distance?

A
  • Light passes through cornea, aqueous humor, lens and vitreous humor on the way to the retina (refracts at each boundary)
  • Lens is adjustable as a stronger lens is required for focus on closer objects
108
Q

What are the scientific names for far and near sighted/?

A

-Myopia (near) and Hyperopia (far)

109
Q

Why do eyes move?

A

-To position the the Fovea (area of retina with most receptors) which is the centre of our gaze. These movements are called saccades and happen multiple times per second.

110
Q

What are the three different eye directions?

A

-Eye moves independently from the head through yaw (each side of the head) pitch (top to bottom of head) and roll (circular)

111
Q

Describe four types of eye movement

A
  • Saccades: move the eye very quickly to a new position between periods of gaze stabilisation (fixations) in order to scan the scene across the entire field of view
  • Smooth pursuit movements: slower, keeps a moving stimulus on the fovea
  • Optokynetic nystagmus: brings the eye back from a peripheral to a more central position after it has followed a large-scale moving stimulus (whilst head is still)
  • Vestibulo-ocular movements: compensate for the movement of the head by moving the eye the same distance but in the opposite direction in order to maintain a constant field of view
112
Q

How is the eye controlled?

A
  • Conscious control comes from cortical frontal eye fields

- Automatic control comes from superior colliculus

113
Q

Describe the characteristics of rods and cones

A
  • Rods= large cells containing large amounts of photopigment, G protein cascade produces high amplification
  • Cones= smaller and have less photopigment, low amplification and recover rapidly from change
114
Q

How are rods positioned within the eye?

A

-Acuity is highest in the Fovea and reduces as you move away. At night acuity is sacrificed for sensitivity so no rods are in Fovea

115
Q

Describe visual transduction

A

-Light causes hyperpolarisation of cell membrane. This activates rhodopsin which then activates G-protein transducin causing Na channels to close making the membrane becoming more polarised.

116
Q

What is opsins role in sensory systems?

A
  • Is a light sensitive protein (g protein coupled receptor molecule) in photoreceptors
  • These ospins vary on cone class being S/M/L each cone absorbs different light wavelengths, all rods have the same type of ospin
117
Q

What are the two main pathways for vision

A
  • Geniculate-striate pathway (retinal projections)

- Extrageniculate pathway (eye movement control and visual processing)

118
Q

What cells detect and influence the sleep/wake cycle

A

-Retinal ganglion cells

119
Q

What is lateral inhibition?

A

-Lateral inhibition occurs where the neurons in a region—in this case, retinal cells—are interconnected, either through their own axons or by means of interneurons, and each neuron tends to inhibit its neighbours. The photoreceptors stimulated by the right edge of each grey bar are inhibited by the neighbouring photoreceptors stimulated by the lighter bar next door. Thus, photoreceptors on the right edge report receiving less light than they actually do

-If the light falling on the group of retinal neurons is uniform, then their reciprocal inhibitions cancel each other out without further effects.
When an edge (dark and light illumination) is created, the cells on both sides of the edge will influence each other strongly. This changes their signals such that a much stronger contrast is coded than physically exists. More distant cells are not affected. As a result the perception of the edge is enhanced.

120
Q

How do cones and rods form a receptive field?

A

-By converging on a bipolar cell through vertical (in the fovea cone to 1 bipolar, periphery cone to multiple bipolar) or horizontal connections (horizontal and amacrine cells)

121
Q

How do on/off bipolar cells work?

A
  • ON-centre bipolar cells have an inhibitory synapse (i.e. IPSPs in presence of glutamate) with those cones (or rods) that form the centre of its receptive field (metabotropic glutamate receptors mGluR)
  • OFF-centre bipolar cells have an excitatory synapse (i.e. EPSPs in presence of glutamate), ionotropic glutamate receptor (iGluR)
  • Light hyperpolarises photoreceptors decreasing glutamate, Bipolar cells can invert this process activating when less glutamate is present or be activated by increased amounts of glutamate (absence of light)
122
Q

How do ganglion cells respond to light rations?

A

Ganglion cells respond to ratios of light/dark, but not to uniform illumination

123
Q

Describe two ganglion cells in the LGN (lateral geniculate nucleus, visual pathway from retina)

A
  • P-ganglion cells (project to Parvocellular layer in LGN) – small receptive fields, slower conduciton speed, high acuity, poor response to transient stimuli, colour sensitive.
  • M-ganglion cells (project to Magnocellular layer in LGN) – large receptive fields, higher conduction speed, sensitive to motion, low acuity, no colour discr
124
Q

How is the V1 (visual cortex) structured

A

-V1 has columnar structure, with neurons segregated into functionally distinct hypercolumns

125
Q

How do simple and complex cortical cells differ?

A
  • Simple cortical cells (aka bar detectors or edge detectors): respond best to an edge or a bar of particular width, orientation, and location in the visual field.
  • Complex cortical cells: respond best to a bad or particular size and orientation anywhere within a particular area of the visual field
126
Q

What are the three types of reduced sensitivity to light?

A
  • Protanomaly: reduced sensitivity to red light
  • Deuteranomaly: reduced sensitivity to green light (MOST COMMON)
  • Tritanomaly: reduced sensitivity to blue light (RARE) – tritanopia: lacking the short-wavelength cones
127
Q

How do mild and severe colour deficiency occur?

A
  • S-cone opsin gene on chromosome 7 while M/L- cone opsin genes on X chromosome (S= short wave ect)
  • Severe= only two cone ospins expressed in retina (lacks cones)
  • Mild= one ospin is mutated and slightly altered resulting in small shifts in spectrum
128
Q

How do different wavelengths affect different cells in the LGN?

A

-Are either activated by certain wavelengths or if they are a spectrally opponent cell have the opposite firing response to different regions of the spectrum

129
Q

How do humans see colour

A

-Trichromaticaly, through three primary colours red(L),blue(S),yellow(M) an equal mix of each is seen as white light

130
Q

What is colour constancy?

A

-Ability to recognise colours under different illuminations

131
Q

How is sound captured and amplified by the ear?

A
  • Sound – pressure waves, movement of air particles set in motion by vibrating structure
  • Measures of sound – frequency (reciprocal of wavelength, perceived as pitch) and amplitude (loudness), phase and waveform
  • Vibrations travel from the tympanum to the middle ear where they are amplified
132
Q

How are sounds processed in auditory pathways?

A
  • Hair cells (non-spiking) are activated through mechanical stimulation of Stereocilium (hair protruding from hair cell) where ion channels are stretched and thus open
  • Bending of the stereocilia (right) opens large, nonselective ion channels, allowing K+ and Ca2+ to enter the stereocilia. The resulting depolarization opens Ca2+ channels in the cell’s base, causing the release of neurotransmitter to excite afferent nerves (linked to CNS)
  • auditory nerve fiber divides into two main branches as it enters the brainstem. Each branch then goes to one of two groups of neurons, one group in the dorsal cochlear nucleus and the other group in the ventral cochlear nucleus. One path from each cochlear nucleus goes to both superior olivary nuclei, so they both receive inputs from both right and left cochlear nuclei. This mechanism plays a key role in localizing sounds by comparing the two ears and is called coincidence detection
133
Q

What are hormones and how do they work?

A

-bioregulators of the endocrine system, secreted by specialised cells directly into the blood, selectively act on target cells (specific to a receptor), change shape of receptor to releases secondary message having a subsequent effect

134
Q

What are the three main types of hormones?

A
  • protein hormones (incl. peptide hormones)
  • amine hormones
  • steroid hormones
135
Q

What is a protein and amine hormone?

A
  • Protein= long chain of amino acids (oxytocin, insulin ect)

- Amine= modified single amino acid (adrenaline, melatonin)

136
Q

Describe the action of hormones

A
  • Bind to specific receptors on outside of cells
  • Act ‘rapidly’ (secs to mins)
  • Can have prolonged effects
  • Sensitivity can be altered by increasing (upregulating) or decreasing (downregulating) numbers of receptors on cell
  • Stored in vesicles and secreted on demand
137
Q

What are steroid hormones?

A
  • Derived from cholesterol, made from four interconnected carbon rings (testosterone, oestrogen ect)
  • Soluble in lipids
138
Q

How do steroid hormones work?

A
  • Bind to specific receptor sites

- Steroid–receptor complex binds to DNA, altering production of proteins

139
Q

Describe the action of steroid hormones

A

-Act on specific receptors inside cells
-Act ‘slowly’ (hours)
Have long-lasting effects via transcription of DNA
-Sensitivity can be altered by presence or absence of co-factors necessary for cells to respond
-Cannot be stored—must be synthesised on demand

140
Q

Where are hormones produced in the body?

A
  • Follicles of endocrine cells secrete hormones into the lumen
  • Hormone transported into thin-walled capillary and flows into bloodstream
  • Ductless—no ducts leading to bloodstream
141
Q

Name three areas of the body that produce hormones and the hormones they produce

A
  • Thryroid gland e.g. thryroxine (increases metabolic rate and promotes growth)
  • Pituitary gland e.g. GH (growth hormone)
  • Pancreas e.g. insulin (decreases blood glucose)
142
Q

What moderates the releases of hormones?

A

-Hypothalamus and pituitary gland

143
Q

How are hormone levels regulated?

A

-feedback loop, often negative (more hormone inhibits production) can be positive

144
Q

Describe four main pathways used as feedback loops

A
  • Autocrine system (secrete a hormone which binds to the releasing cell causing it to change)
  • Target cell feedback (the effect on the target cell causes changes in releasing cell e.g. insulin pathway)
  • Brain regulation (similar to target cell but effect is communicated to the brain e.g. hypothalamus and fight or flight response)
  • Brain and pituitary regulation (feedback loop communicates to both the brain and pituitary gland e.g. temperature regulation to pituitary and hypothalamus)
145
Q

What are the two parts to the pituitary gland

A
  • anterior= synthesises and secretes

- Posterior= stores and secretes

146
Q

Describe the the short and long term effects of hormones

A
  • Oxytocin and milk letdown reflex (nerve impulses from sucking stimulate hypothalamus) (S)
  • Growth hormone and bone growth (L)
147
Q

What are the five ways hormones affect behaviour and provide an example for each?

A
  • Biological rhythms (melatonin from pineal gland in wake/sleep cycle)
  • Eating and drinking (Ghrelin secreted by the stomach to stimulate feeding)
  • Reproductive behaviour (menstrual cycle
  • Social behaviour (oxytocin and increased maternal behaviour in rats/ increased generosity & trust in humans Zak et al 2007, Kosfield et al. 2005)
  • Stress
148
Q

Hoe can hormone effects be tested for?

A

-Placebo double blind trial, refer to Zak et al. 2007 oxytocin nasal spray and generosity

149
Q

Name key differences and similarities between the endocrine and nervous system

A
  • Both= communicate and control systems and can be influenced by prior exposure
  • Different= conveyed chemically/action potential, in blood/ nerve fibre, slow/fast, short-lived/persists
150
Q

What is stress?

A

-situation that upsets an animals homeostatic balance

151
Q

What two systems are activated by stress?

A
  • sympatho-adrenergic system (SAS)

- hypothalamic-pituitary-adrenal (HPA)

152
Q

What are the three stages of a stress response?

A
  • Selye’s general adaptation syndrome
  • alarm (perceived by pituitary adrenal system, SAS prepares for fight or flight, HPA releases energy stores)
  • resistance (balance is tried to be obtained unless stressor persists)
  • recovery/exhaustion (stress depletes resources and bodies defences, stress illness can develop)
153
Q

Describe the role of the SAS

A

-Activates adrenal medulla which then releases adrenaline and noradrenaline (norad= stimulates alpha receptors in muscle redirecting blood to essential organs and increases blood pressure/ adren= raise heart rate and blood flow to muscles, dilates pupils, glycogenolysis in which blood sugar is raised)

154
Q

Describe the role of the HPA

A

-ACTH stimulates release of cortisol and other steroids to engage slower acting, passive coping mechanisms e.g. directs oxygen and nutrients to the brain, lipolysis process that breaks down fats, gluconeogenesis process of increasing glucose, suppresses immune system.

155
Q

how does the exhaustion stage lead to stress related illnesses?

A

-Sustained use of HPA causes hypertension (high blood pressure), digestion is suppressed leads to irritable bowel syndrome, reproduction is suppressed can lead to impotence, immunity being suppressed makes disease and illness in general more likely

156
Q

Name two types of stressors

A
  • Systematic stressors (actual threats)

- Neurogenic stressors (anticipated threats)

157
Q

What can cause chronic stress?

A

-Frequent, high rates of stress related to things such as occupation, finance ect

158
Q

What is the difference between eustress and distress?

A
  • Eustress= beneficial stress where homeostasis is restored easily restored
  • Distress= harmful and can lead to abnormal behaviour
159
Q

Explain transactional theory

A
  • Dynamic relationship between stressors in the environment and individuals psychological resources to cope/deal with them
  • Stress comes as a result of of an imbalance between the two
160
Q

Describe the concept of cognitive appraisal

A
  • Process which decides if there is a threat and if that threat can be dealt with, process which leads to no stress, eustress or distress
  • Primary appraisal= significance in terms of personal goals, values, self-beliefs (is situation relevant and threatening or beneficial to me)
  • Secondary appraisal= ability to control situation and wellbeing (what can/should be done)
161
Q

Is there evidence for stress immunisation?

A
  • Yes, small amounts of stress in early life can lead to greater resilience
  • Mirescu et al. (2004) observed this in rat pups, being handled increases stress and as adults where more resistant to stress
162
Q

What are genes?

A

-Located on chromosomes in cell nucleus and help code for production of proteins (antibodies, enzymes, hormones ect)

163
Q

What is the difference between a genotype and phenotype?

A
  • Geno= set of genes a person possesses

- Pheno- observable characteristics of an individual influenced by genes and environment

164
Q

What is an allele?

A
  • Variants of a gene such as eye colour. Some are more dominant than others.
  • Expression of these alleles can be homozygous if parents posess the same allele or heterozygous if they differ (dominant one expressed)
  • Some alleles are lethal and can reduce the number of homozygous recessive offspring (yellow coated mice)
165
Q

What is polygenic inheritance?

A

-Multi gene inheritance e.g. skin colour is decided from a combination of eight different gametes (combination of alleles)

166
Q

What are the challenges of behavioural genetic research?

A
  • difficulty in defining and quantifying behaviour
  • environmental influences on behaviour
  • within- and between-individual variation in behaviour
  • involvement of many genes
  • different genes function in different tissues at different times during the development of an organism
167
Q

Outline a studie that show the influence genes have on behaviour

A

Weber et al. (2013) Deer mouse builds no escape tunnel in burrow, oldfield mouse does. Bred together, F1 (first generation) all built escape tunnel, bred again with deer mouse, 50% built escape tunnel. Shows there is a single dominant allele for buidling escape tunnel.

168
Q

What is the norm of reaction?

A

-Pattern of phenotypic expression of a single genotype across a range of environments

169
Q

How is trait heritability determined?

A

-proportion of phenotypic variance associated with genetic variance

170
Q

How is phenotypic variance determined?

A

-effects of genetic variance associated with environmental variance

171
Q

Outline a study to show how selective breeding can be implemented and how environmental effects can influence expression of the selected trait

A
  • Rat study which bred rats that were better at completing mazes
  • However when compared to ‘dull’ rats in a restricted environment both were equal in terms of completing a maze (restricted environment restricted expression of the trait)
172
Q

What is the difference between a wild type allele and a mutant allele?

A
  • Wild type= greater than 1% frequency of expression

- Mutant= less than 1% frequency of expression

173
Q

What is the difference between a monomorphic and polymorphic wild type allele?

A
  • Mono= one wild type allele

- poly= more than one type of wild type allele

174
Q

Give an example of a mutant gene study

A

-Social amnesia, couldn’t remember familiar rats, study (result of single gene mutation)

175
Q

What is non-genetic inheritance with an example

A
  • Factors in one individual influence the behaviour or development of another individual (without passing on genes) who, in turn, may pass on these influences to another
  • Bower bird watches other males build nest to learn nest building skills
176
Q

What is vertical transmission of non-genetic behaviour?

A

-Between generations transfer but can skip generations (unlike genetic inheritance) e.g. bird teaching offspring bird call

177
Q

What is horizontal transmission of non-genetic behaviour?

A

-Within generations, from peer to peer e.g. birdsong between neighbours

178
Q

How do maternal effects teach behaviour

A

-Phenotypical expression on genes influences behaviour (can be pre and post birth e.g. food mother rabbit eats during pregnancy is prefered by offspring (pre)/ what plant white butterfly lays eggs on is preferred by offspring when laying eggs (post)

179
Q

What is social learning/

A
  • learning that is facilitated by observation of, or interaction with, another individual or its products Hoppitt & Laland (2013)
  • ‘observer’ individual learns from ‘demonstrator’ individual
  • differs from individual learning because it is heritable
180
Q

Why does social learning occur and why does it not always occur?

A

For=
-may be less time-consuming than individual learning
-may allow exploitation of new resources, e.g. by overcoming neophobia (fear)
-may be less risky than individual trial-and-error learning
Against=
-may sometimes be more time-consuming to wait for conspecifics than find out yourself
-actions of others may be outdated or not relevant to your needs
-individual learning can sometimes yield higher pay-offs

181
Q

Describe the five mechanisms of social learning?

A
  • Local enhancement (draws attention to specific location where behaviour is occurring)
  • Stimulus enhancement (draws attention to object or stimulus which is then generalised)
  • Observational conditioning
  • Imitation
  • Goal emulation
182
Q

What is cultural transmission of behaviour?

A

-Behaviour techniques are transmitted socially over many generations

183
Q

What is symbolic representation in learning behaviour?

A
  • The use of arbitrary symbols to represent (or stand for) objects and actions
  • When two initially unrelated stimuli are associated with the same event, an emergent relation can develop such that they become interchangeable in other contexts e.g. human language and signs/ bees and tail waggle to indicate nectar
184
Q

What are the two types of hormone effects in contrast to sex differences

A
  • Organised effects= effects on tissue differentiation and development, permanent
  • Activational effects= effects that occur in fully developed organism, transient
185
Q

What are sexual dimorphisms?

A

-Differences between males and females that are anatomical, physiological and behavioural as a result of organised effects

186
Q

Describe the genetic basis of sex differentiation

A
  • Sex is genetically determined
  • diploid human cells contain 46 chromosomes (23 pairs) one of these pairs determines sex
  • Gametes are one copy of each chromosome (two gametes is one diploid) fusion of these gametes create diploid offspring (e.g. gamete x and gamete x create diploid offspring xx)
  • Sex is determined by male gamete (females gamete is always x)
187
Q

Describe gondal sex differentiation

A
  • Gonads are either exposed to SRY gene or not
  • Presence of this gene sets off production of SRY protein causing chain reaction resulting in testis
  • No SRY causes default sex (female) and development of ovaries
  • Early embryonic development is effected by this process. Ovary does not produce significant amount of steroid hormones, body develops to own intrinsic programme. Testis produce testosterone and AMH masculinises tissue brain and internal genitalia
188
Q

Describe how phenotypic sex is decided?

A
  • Genotypic sex determines gondal sex which then determines phenotypic sex
  • Sex steroids permanently (released in puberty and foetal dev) cause differences in sexual differentiation of body, brain and behaviour
189
Q

Explain how sex steroids cause masculinisation and de-feminisation

A
  • AMH = masculinises internal genitalia
  • DHT= causes development of male external genitalia
  • Testosterone= masculinises rest of body (brain ect)
190
Q

What happens at puberty?

A
  • release of growth hormone, gonadotropic hormone and adrenocorticotropic hormone causes development of secondary sexual characteristics (breasts, facial hair, acne, hair recession, menstruation
191
Q

Describe sex differences in the brain

A
  • Testosterone creates male behaviour e.g. guinea pigs and rhesus monkeys given testosterone when pregnant or to newly born offspring showed male behaviour such as preference for females (depsite being female)
  • Sexually dimporhic brain structures e.g. bigger hypothalamus in male rats made smaller in castrated males (lack of test) and larger in females given test
  • Male brains in humans are heavier and heavier relative to body size (unclear the consequences or function of this)
  • Brain lateralisation in females is weaker