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PS2001 > Behavioural neuroscience > Flashcards

Behavioural neuroscience Flashcards

1
Q

what is phrenology

A

physical functions can be localized to different areas of cortex
so the brain is like a muscle - bits you use more get bigger and stronger

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2
Q

history of neuropsychology

A

gall 1800 first attempts to bring together biological and physiological concepts in the study of behaviour
alot of this is now very outdated

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3
Q

what is the aggregate field hypothesis

A

flourens 1850s
removed gall’s phrenological centres
concluded any part of the cerebral hemisphere could perform any higher function

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4
Q

why was the aggregate field hypothesis a popular theory

A

went against the reductionist idea that the human mind has biological basis
so was pro religion

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5
Q

how and who refined the aggregate field hypothesis

A

mass action
karl lashley 1900
size of brain lesion defines deficit not location

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6
Q

key concept behind distributed processing

A

individual areas of the brain perform specific functions but complex cognitive function involves interactions of many brian areas

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7
Q

ideas / evidence behind distributed processing - whats special about how they studied

A

Brocca - 8 patients with similar brain lesions who could not produce speech
wernicke - described patients with an inability to comprehend language
both studied patients deficits whilst alive then disected the brain once dead to find specific areas

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8
Q

the neuron doctrined

who and what

A

camillo golgi and santigo ramon y cajal

the neuron is the signalling unit of the brain

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9
Q

what is cellular connectivity

A

the idea neurons are organised into functional groups which are interconnected by specific neural pathways

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10
Q

what makes up a neuron

A 
think of picture
soma - cell body
dendrities off the cell body
axon inside the myelin sheath
terminal buttons
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11
Q

in which direction does information travel around a neuron

A

from the dendrites on the soma to the terminal buttons

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12
Q

how are proteins moved around the neuron

A

vesicles walk proteins along microtubules

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13
Q

what are the threetypes of neurons

A

multipolar and biopolar and unipolar neurons

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14
Q

what are multipolar neurons

A

the most common type

soma, axon, terminal buttons

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15
Q

what are bipolar neurons

A

receptor on the dendrite - cilia are sensitive to physical stimuli
soma is then halfway along the axon
terminal buttons at the end carrying information towards the brain

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16
Q

where are bipolar neurons usually found

A

in sensory systems

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17
Q

what are unipolar neurons

A

many dendrites sensitive to physical stimuli
soma is separately attached halfway along the axon
terminal buttons carrying information towards the brain

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18
Q

where are unipolar neurons usually found

A

in the somatosensory system (warmth, pain etc)

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19
Q

how do neurons communicate with each other

A

action potentials

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20
Q

what is the resting potential of neurons and why (membrane potential)

A

-70mV
the force of diffusion vs
the force of electrostatic pressure (charges repelling)
the resting potential is due to a difference in the concentration of positively charged ions inside the neuron relative to the outside of the neuron

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21
Q

what are action potentials

A

a brief electrical impulse that provides the basis for conduction along an axon

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22
Q

what chemicals are usually intra and extra cellular

A

intra - A- (anions) and K+

extra - Cl- and Na+

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23
Q

where are axon potentials generated

A

in the cell body

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24
Q

what are the 6 steps to an action potential

A

1 Na+ channels open and Na+ begins to enter cell
2 K+ channels open, K+ begins to leave the cell
3 Na+ channels become refractory, no more Na+ enters the cell
4 K+ continues to leave the cell, causes membrane potential to return to resting level
5 K+ channel closes, Na+ channel resets
6 Extra K+ outside diffuses away
try put with diagram where 3 is the height of the action potential

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25
Q

what happens to action potentials as they are propogated down the cell

A

they don not change size

they are continually regenerated by ion channels along the axon

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26
Q

how is the resting potential restored after and action potential

A

by voltage dependent potassium channels

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27
Q

consequence of action potentials in terms of speed and energy

A

using ion channels to generate action potential is slow and uses energy
signal travels faster down insulated axons but it reduces in size and so needs to regenerate periodically

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28
Q

how are action potentials regenerated

A

saltatory action

action potentials are regenerated at nodes of ranvier - the gaps between the myelin sheaths

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29
Q

how much if the CNS do neurons make up

A

half the volume of the cns

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30
Q

what makes up the other half of the volums of the cns if not neurons

A

glia cells - supporting cells

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31
Q

3 main types of glia cells

A

oligodendrocytes
astrocytes
microgli

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32
Q

what do oligodendrocytes do

A

provide support from neurons and produce myelin

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33
Q

what do astrocytes do

A

housekeeping duties, support and insulation
provide energy in the form of lactate
small quantity of energy stored as glycogen
removal of dead tissue through phagocytosis
(these are the most well studied)

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34
Q

what do microglia do

A

inflammatroy response to infection and removal of dead tissue

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35
Q

what are the two ways we measure communication between neurons

A

electrically - neurophysiology
- branch of physiology that deals with the flow of ions in brain tissue and the measurement of that flow
chemically - microdialysis
- allows measurement of levels of chemicals (glucose, neurotransmitters) in the brain

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36
Q

how does microdialysis work

A

same way as standard dislyss
probe implanted into the brain (so only really possible to carry out on animals)
fluid pumped through inner cannula
neuro transmitters from extracellular fluid diffuse into dialysis tubing \we can measure this fluid and detect the changes

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37
Q

problem with microdialysis

A

takes a long time

if interested in cognition where we need measurements in millisecond intervals this is a problem

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38
Q

4 types of electrophysiology

A

electroencephalogram - EEG
single cell recording
multi-cell recording
intracellular

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39
Q

advantages of EEG

A

non invasive so can use in humans

high temporal resolution

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40
Q

disadvantages with EEG

A

low spatial resolution

only record from the cortex

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41
Q

example of the use of EEG

A

medically study sleep and pinpoint the focus of seizure activity in epilepsy

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42
Q

what is multi cell recording

A

used to record groups of neurons
record brain rhythms (local field potential LFP)
think of it like a crowd at a concert
if the crowd sings together then the song is recogniseable
so if neurons fire together this produces waves of activity that can be detected in other areas of the brain - co-ordinate different brain areas

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43
Q

advantages of multi-cell recording

A

ok spatial resolution (groups of neurons)

ok temporal resolution (brain rhythms)

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44
Q

disadvantages of multi-cell recording

A

only records groups of neurons

is invasive

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45
Q

example of how multi-cell recording can be used

A

in rats

memory and attention networks coordinate when rats use memory to make a decision

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46
Q

advantages of single-cell recording

A

very high spatial resilution (multiple single neurons)

high temporal resolution (action potentials!)

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47
Q

disadvantages to single-cell recording

A 
extracellular recording (no knowledge of intracellular events)
invasive
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48
Q

advantages of intracellular recording

A

very high spatial resolution (specific neuron)

examine sub-cellular processes

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49
Q

disadvantages of intracellular recorgind

A

only one cell at a time

only in anaesthesised animals

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50
Q

example of use of intracellular recording

A

allowed us to understand how action potentials worked

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51
Q

if action potentials are always the same size, how do neurons communicate with one another

A
  • frequency is important and not size. stronger stimulus = more action potentials
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52
Q

where and how do neurons communicate

A

across synapses
neurotransmitters are released from the pre-synaptic membrane of the terminal button
entry of calcium opens fusion pores
pores widens, membrane of synaptic vesicle fuses with presynaptic membrane
molecules of neurotransmitter leave terminal button

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53
Q

where do neurotransmitters ac on post-synaptic receptors

A

on the dendrites

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54
Q

what are the two main types of receptor for neurotransmitters acting on post-synaptic receptors

A

ionotropic

metabotropic

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55
Q

how ionotropic receptors work

A

they transmit information quickly

relatively simple mechanism

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56
Q

how do metabotropic receptros work

A

slow acting and long lasting

complex mechanism

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57
Q

what are the two types of neurotransmitter

A

excitatory

inhibitory

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58
Q

how excitatory neurotransmitters work

A

causes depolarisation - produces actionpotentials
alos known as excitatory posy-synaptic potential
eg glutamate

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59
Q

how inhibitory neurotrasnmitters work

A

causes hyperpolarisation - stops action potentials being generated
also know as an inhibitory post-synaptic potential
eg GABA

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60
Q

what causes inhibition or excitation at the post-synaptic membrane

A

not the neurotransmitter!

the ion channel the neurotransmitter opens

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61
Q

which ion channels opening causes depolarization (excitation)

A

na+

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62
Q

which ion channel opening causes hyperpolirisation (inhibition)

A 
K+ = efflux so goin out of the cell
Cl- = influx so going into the cell
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63
Q

what is neural integration

A

all the time our neurons are procesing lots of information
enough excitation over threshold = action potential down axon
whilst still some residual excitation, next signal is inhibitory do no action potential
so neurons integrate excitation vs inhibition
IPSPs counteract EPSPs so action potential is not triggered in axon

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64
Q

what are the two theories of how neurons work tigetherq

A

referendum style - point neuron hypothesis
one synapse one vote
each synapse has equal weighting in a neuron. neurons will fire if ecitatroy input is greater than inhibiroty
OR
general election style
two compartment hypothesis
neurons split into 2 funcitnoal compartments
1 - soma, basal dendrites, axon
2 - apical dendrite tree
sum of inputs from apical dendrites passed onto soma
(More compartments?)

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65
Q

psychopharmacology - definition

A

the study of the effects of drugs on the nervous system and behaviour

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66
Q

uses of psychopharmacology

A

medicine
illegal drugs trade\cognitive enhancers
tool to study the mechanisms by which the brain controls psychological function
tool to study the mechanisms by which the brain controls psychological functions

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67
Q

agonist definition

A

a drug that facilitates the effects of a particular neurotransmitter on the postsynaptic cell

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68
Q

antagonist

A

a drug that inhibits the effects of a particular neurotransmitter on the postsynaptic cell

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69
Q

what is special about apomorphine

A

can be either an antagonist or an agonist depending on the dosage (relates to dopamine production)

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70
Q

glutamate and gamma-aminobutyric acid

A

most common neurotransmitter in the brain

nearly all neurons recieve inputs from GABA

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71
Q

what are the 4 types of glutamate receptor

A

NMDA
kainate
AMPA
metabotropic glutamate

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72
Q

what are the two types of GABA receptor

A

GABA little A (ionotropic)

GABA little B (metabotropic)

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73
Q

where are the signals usualy from in neural integration

A

glutamate and GABA inputs

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74
Q

what do other (not GABA and glutamate) neurotransmitter systems do

A

also produce action potentials in postsynaptic cells
neuromodulatorye effects
can increase or decrease the likelihood of glutamte or GABA release producing an action potential in the postsynaptic cell

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75
Q

Acetylcholine (ACh)

A

two types of ACh receptor: nicotinic (ionotropic) and muscarinic (metabotropic)
nicotinic receptors found in the brain responsible for nicotine addiction
also found in the muscles - these are blocked by botox injections
muscarinic cholinergic receptors found only in the brain

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76
Q

what are the three main systems of ACh (no explanation)

A

dorsolateral pons
basal forebrain
medial septum

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77
Q

dorsolateral pons system and ACh

A

traditionally associated with sleep
recently shown to play a role in higher cognitive functions like learning - rats with cholinergic lesions of the dorsolateral pons cannot learn the association between reward and location

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78
Q

basal forebrain system and ACh

A

provides large input to the cortex and has a role in learning and attention
historically studied as this area degrades in alzheimers. most treatments still try to fix the imbalance of ACh

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79
Q

medial septum system and ACh

A

involved in learning and memory
controls rhythsm in the LFP in the forebrain
lesions of the medial septum get rid of the LFP rhythm in the hippocampus

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80
Q

information about the dopamine system

A

catecholamine along with noradrenalin

at least 5 receptor sub types (D1-5) which are all metabotropic

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81
Q

3 major dopaminergic systems in the brain

A

nigrostriatal

mesolimbic mesocortical

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82
Q

path of nigrostriatal dopaminergic system in the brain

A

substanti nigra
caudate nucleus/ putamen
contorls action selection and coordinated movement

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83
Q

path of mesolimbic dopaminergic system in the brain

A

ventral tegmental area
nucleus accumbens
processing of reward

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84
Q

path of mesocortical dopaminergic system in the brain

A

ventral tegmentl area
prefrontal cortex
short term memory and planning

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85
Q

how have the role of mesolimbic dopamine system in behaviour signals been studied

A

using single-cell recording
dopaminergic neurons respond to the reward (primary reinforcer) during learning but this decreases as the animal learns the task
when the task is well learned the dopamine neurons respond to the cue (secondary reinforcer)

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86
Q

noradrenergic system

A

catecholamine (also called neuroepinephrine
4 types of receptors alpha 1 and 2, beta one and 2, all metabotropic
most important noradrenergic system originates in the locus coeruleus - involved in vigilance and attentiveness

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87
Q

serotinergic system

A

indolamine
at least 9 receptor subtypes - most are met\botropic
most important serotinergic system originates in the raphe nuclei of the midbrain and pons
functions are complex; regulation of mood, eating, sleeping and pain

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88
Q

what is neuromodulation

A

many of the systems all originate in relatively small nuclei in the brainstem and midbrain
they all send projection over the forebrain
activztion of these small areas of the brain can then have large impacts on the rest of the brain

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89
Q

are neurotransmitter systems independent and example

A

no
hippocampus
neurons predominantly use glutamate and GABA to transmit info
hippocampal neurons also modulate ACh and dopamine
to fully understand the function of the hippocampus the combined actions of these systems must be studied

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90
Q

rats learning food locations trial

A

rats can learn new food locations in the map in one trial
they spend more time digging in the correct locatin
these new memories are dependent on glutamate activity in the hippocampuse
we know this as when glutamate activity is blocked with pharmocology, they do not remeber the location of the food
block dopamine in the hippocampus you get similar effects
shows the interaction between neurotransmitter systems

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91
Q

sleep in the animal kingdom

A

sleep is seen throughout the animal kingdom

variation in sleep patterns

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92
Q

dolphin’s adaptation to sleep

A

bottlenose dolphins - sleep one hemisphere at a time

indus dolphins - never stop swimming but still sleep in brief 4-60s naps

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93
Q

sleep in humans

A

amount of sleep needed changes with age
no adapttion to sleep deprivation
very different to unconsciousness (coma / anaesthetic)

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94
Q

how the stages of sleep in humans work

A

awake = little alpha and beta
stage 1 = a little theta activity
stage 2 = k complex and sleep spindle
stage 3 = delta activity
stage 4 = loads of delta activity = slow wave sleep
REM sleep = theta activity and beta activity

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95
Q

REM vs slow wave sleep

A

REM is characterised by EEG desynchrony, lack of muscle tone (paralysis), and rapid eye movement
SWS is characterised by EEG synchrony, moderate muscle tone and absence of eye movement

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96
Q

sleep cycle

A

awake,1,2,3,4,3,2,1,REM,1,2,3,4… etc

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97
Q

disorders of sleep general information

A

affects 25% of the population (9% regularly)
self report is extremely unreliable
pharmalogical treatments

98
Q

sleep apnea

A

stop breathing whilst asleep
treated surgically or by wearing pressurised breathing apparatus
can cause permanent damage

99
Q

narcolepsy

A 
primary symptom = sleep attack
cataplexy = brief conscious paralysis
sleep paralysis
hypnagogic hallucinations
genetic component causes loss of hypocretin / orexin neurons
treated with modanfinil
100
Q

REM sleep disorder

A

paralysis that normally appears during REM sleep is not present - people act out their dreams
genetic disorder involving accumulation of alpha synuclein in neurons
treated with benzodiazepine

101
Q

name some disorders of slow wave sleep

A

sleep walking
bedwetting
night terrors
all associated with childhood and usually diminish with age
sleep eating disorder?? thought to be induced by sleeping medication so treatments involve refining this medication

102
Q

how are levels or arousal controlleed

A 
by a collection of modulatinf neurotransmitter systems usually in the brainstem 
eg
ACh
noradrenalin
serotonin
histamine
orexin
103
Q

where is histamine found

A

hypothalamus

104
Q

when are noradrenalin neurons active

A

during waking

not active during sleep`

105
Q

when are serotonin neurons active

A

active during waking hours and less active during sleep

106
Q

when are orexinergic neurons active

A

active during waking and not during sleep

107
Q

what is the flip-flop switch

A

switch of mutual inhibtion between ventrolateral preoptic area and the arousal systems (ACh, noradrenalin, serotonin, histamine)

108
Q

control of REM sleep

A

second flip-flop switch to turn on REM
REM-on cells (ACh) found in sublaterdoesal nucleus in the dorsal pons
REM-off cells found in the ventrolateral periaqueductal gray matter
the REM off neurons get input from arousal system keep them active
REM-off neurons become gradually less active as the excitation from the arousal system deceases
when the off cells become less active the switch flips and the ACh REM-on neurons become active

109
Q

what does sleep deprivation do

A

mainly affects cognitive abilities
we do not make up lost sleeo
following deprivation SWS and REM dominate

110
Q

Rechtschaffen and Bergmann 1995 - sleep deprivation in rats what did they find

A

metabolic rate in sleep deprived rats increase to between 210-270% of normal levels
weigh loss despite increased food intake
inability to thermoregulate (excessive heat loss)
death after 2-3 weeks

111
Q

function of SWS

A

reduced metabolic rate and blood flow rely on rest?
most active regions during waking show highest delta wave activity during SWS
cortex shuts down
protect free radicals and oxidative stress

112
Q

what happens during sleep to protect the brain`

A

sleep drives metabolite clearance from the adult brain

113
Q

what penetrates much further into the brain during sleep - why

A

CSF

toxic chemicals such as amalyoid beta are removed quicker during sleep

114
Q

function of REM sleep

A

is seen the most in most active phases of brain development
more prevalent in new born animals with less well developed brains than animals born with well developed brains
if merely development related why do we see it in adults
learning and memory?

115
Q

what is declarative memory

A

memory that can be consciously recalled

116
Q

what is non-declaritive memory

A

automatic learning not under conscious control (eg riding a bike)

117
Q

mednick et all 2003 - what was their sleep experiment

A

is sleep important for non-declarative memory

found REM sleep facilitates perceptual leraning

118
Q

tucker et al 2006 - what was their sleep experiment

A

paired associate task - declaritive memory

SWS facilitates declarative learning

119
Q

what are the mechanisms during sleep that improve memory

A

place cells

120
Q

name the four types of biological rhythms

A

ultradian
circadian
infradian
circannual

121
Q

ultradian rhythms

A

multiple cycles within a 24hr period eg appetite

122
Q

circadian rhythms

A

24 hr cycles eg sleep-wake

123
Q

infradian rhythsm

A

longer than 24hr eg menstruation

124
Q

circannual rhythm

A

year long cycle eg hibernation

125
Q

control of circadian rhythms

A

suprachiasmatic nucleus - lesions here disrupt the timing of sleep but quality is unchanged
recieves input from the retina
melanopsin containing ganglion cells are sensitive to light and connect the retina to the SCN
SCN projects indirectly to the VLPA and the orexin neurons of the lateral hypothalamus

126
Q

what neurons have an internal mechanism that allows them to keep track of time
how do we know this

A

SCN

cells raised in culture have 24hr cycles of activity but they are offset from each other - ie are not in time

127
Q

rhtyms are controlled by…

A

at least 7 proteins

pulses of light can reset the protein levels

128
Q

how are infradian rhythms controlled in mammals

A

pineal galdn secrets melatonin
melatonin is secreted at night - longer nights mean higher melatonin levels = winter cycles
also some role in circadian (jet lag cure) and seasonal affective disorder

129
Q

name 6 neurodegenerative disorders

A 
parkinsons
alzheumers
huntingtons
amyotrophic lateral sclerosis
multiple sclerosis
neurological disorders
130
Q

parkinsons disease - why, how many effected

A 
loss of dopamine neurons from the midbrain 
relatively common (2-3% of pop over 65, 3-4% over 85
131
Q

parkinsons symptoms

A 
muscle rigidity
akinesia - inability to initiate movement
bradykinesia - slowness of movment
resting tremor
cognitive deficits?
132
Q

pathology of parkinsons

A

loss of the substantia nigra pars compacta
symptoms do not occur till 70% of DA neurons are loss
more loss from putamen than caudate nucleus
presence of lewy bodies in the cytoplasn of neurons = an index of neurodegeneration

133
Q

what causes the symptoms of parkinsons

A

by excessive inhibitory activity in the basal ganglia

134
Q

treatment for parkinsons and side effects
- also mention the experimental treatments
4 in total

A

L-DOPA = dopamine precursor
dopamine agonists to increase dopamine acticity
side effects
tardive dyskinesia (uncontrolled movements)
becomes less effective with time as it is not treating the cause and dopamine neurons are still being lost
OR
replace lost dopamine cells
-surgical implantation of fetal dopamine tissue
-stem cells
some positive results but also made some patients much worse so treatment no longer used
OR
lesion in global pallidus (internal segmentum)
OR
deep brain stimulation
OR potential for gene therapy as 5% of cases have a genetic cause

135
Q

alzhiemer’s what is it characterised by and how many effected

A

characterised in its late stages by a general cognitive decline including deficits in memory, attention,language and spatial orientation
10% of pop over 65
50% of pop over 85

136
Q

brain degeneration in alzheimers

A

starts with degeneration in the enthorhinal cortex but damage spreads through the hippocampus, neocortex into the modulatory system of the midbrain and pons

137
Q

what are the biological makers of alzheimers

A

extracellular plaques made from the accumulation of the 40/42 amino acid beta-amyloid peptide
intracellular accumulation of neurofibrillary tangles mades from hyperphosphorrylated tau

138
Q

treatment for alzheimers disease

A 
drug therapy (ACh inhibitors, NMDA receptor antagonist memantine)
these do nothing to treat the cause
at least some cases are genetic (eg mutation in the presenilin gene results in AB production)
most cases do not have an obvious genetic cause
vaccination against AB protein
139
Q

decrease in AB correlated with ….

how does this relate to vaccines

A

correlated with slowing dementia
further studies have shown AB can be reduced by immunisation
but this isnt correlated with slowing dementia so makes the role of AB unclear

140
Q

huntingtons disease
background
who / how many

A

entirely hereditary
results from single genome on chromosome 4 which causes a protein called huntingtin (htt) to be produced
critical feature is a segment of repeated glutamine within the protein
affects the basal ganglia
symptoms include congitive deficits and uncontrollable movements
approx 5,000 people in the uk

141
Q

key bio features of huntingtons

A

inclusion bodies (accumulation of htt)
role of these inclusion bodies is debated
could be neuroprotective

142
Q

what is amyotrophic lateral sclerosis also known as

A

motor neuron disorder

143
Q

motor neurons disorder

  • what
  • death
  • treatment
A

progressive disorder attacking the spinal and cranial nerve motor neurons
no cognitive decline
death usually occurs after 5-10 years after onset as a result of respiratory muscle failure
no effective treatments
riluzole used to reduce glutamate neurotxicity but this only extends life by a few months

144
Q

multilpe sclerosis

A

autoimmune demyelination
damage occurs in white matter located throughout the brain and spinal cord resulting in a variety of disorders
patients may suffer discrete attacks or a more progressive decline
life expectancy is reduce by 5-10 years

145
Q

what causes tumors

A

uncontrolled and non-functional cell division

146
Q

how do tumors cause damage

A

compression and infiltration

147
Q

how are tumors treated

A

surgery and focused radiation

148
Q

meningioma and glioma

which are malignant and which are benign

A

men - benign

glioma - malignant

149
Q

two types of cerebrovascular accidents and what are they

A

hemorrhagic stroke - burst blood vessel

obstructive stroke - blood vessel blocked

150
Q

how do cerebrovascular accidents cause damage

A

very quick depletion of oxygen and glucose
ion transporters disrupted and cells become depolarised
glutamate is produced producing a cycle of excitation and cells die through excessive sodium and calcium within the cell
damaged mitochondria then produce free radicals which are extremely toxic (attack proteins and DNA)

151
Q

how are strokes treated

A

with drugs aimed at dissolving blockages

152
Q

quick diagram to explain short vs long term memory

A 
sensory info
leads to
short term memory      
leads to       (this line is called consolidation), loop from here back to short term memory which is called rehersal                       
long term memory
153
Q

how could you define short term memory in terms of long term memory

A

short term memory (also called working memory) is the gateway for information to enter long term memory

154
Q

explain the long term memory systems

A 
long term memory
declaritive vs non-declaritive
inside declaritive
episodic and semantic
inside non-declaritive
procedural (skill), priming and perceptual learning, non-associative learning, classical conditioning
155
Q

what is priming

A

improvement in identifying or processing a stimulus as a result of its having been observed previously
priming increase the probability of choosing previously presented words for example

156
Q

classical condition as part of memory

A

previously neutral stimuli (CS) is paired with a positive or negative stimulus (US) that produces a response (UR)
in subsequent trials the CS can illict a conditioned response which is very similar to the UR in the absence of the US

157
Q

what is non-associative learning

A

learning that does not involve the association of two stimuli to illicit behavioural response
habituation - decrease in level of response through repeated exposure to a stimulu
sensitisation - increase in level of response through repeated exposure to a stimulus

158
Q

two types of declaritive memory explained

A

sematic - memory for facts

episodic - memory for events

159
Q

why is studying episodic memory important?

A

first symptom of mild cognitive impairment which often preceeds alzheimers
have a;sp recently been described in huntingtons following chemo and after ECT for depression
to understand the mechanisms underlying these disorders we need to understand the neural circuitry that supports episodic memory
hippocapus involved - we know because of HM

160
Q

hippocampus is critical for….

A

episodic memory in humans

161
Q

what is the big question surrounding episodic memory

-why does it matter

A

do animals have it

if they do then we can test new treatments for the early stages of AD

162
Q

definition of episodic memory

A

receives and stores information about temporally dated episodes or events and the temporal-spatial relations among these events - tulving (what, where, when)
then autonoetic conscious later got added to this definition

163
Q

example of episodic type memory in animals

A

scrub jays chose the worms when they are fresh but know they will be bad if return too long later so instead go for the other food
so the scrub jays can do what where and when

164
Q

why are birds not a good model for neuroscience

A

brains are quite different from mammalian brains - hard to use homologous approach
very little known about their brains and behaviour (although this is changing)
good to study convergent evolution of psychological processes

165
Q

do rats have episodic-like memory

A

they can do where but not when
how much do we use actual time
context?
what where and which might be more appropriate

166
Q

lesions in rats show

A

hippocampus is vital for episodic type memory

167
Q

what are the cellular mechanisms for memory consolidation

A

synaptic plasticity
learning must involve chmages in synaptic function
for long-term memory these changes must be long lasting
LTP

168
Q

chemistry of short term LTP

A

dependent on NMDA receptors which allow Ca2+ ions into the cells once activated
these ions set in motion a cascade of reactions that result in more AMPA receptors being inserted into the postsynaptic membrane
more AMPA recpetors result in a stronger response to stimulation from the preseynaptic cell
synapse strenghten for a few hours - short term LTP

169
Q

chemisty of long lasting LTP

A

requires proteins to stabilise short term chages already produced
these are captured by tags that are set at the releant synapse

170
Q

for long lasting memory we need long lasting…

and explain

A

LTP
for this we need
short term LTP (insertion of AMPA receptors into postsynaptic membrane)
a chemical tag at the synapse to attract proteins
proteins to stabilise the changes induced in short term LTP

171
Q

what is hebbs law

A

cells that fire together wire together

172
Q

spatial memory is part of what type of memory

A

episodic

173
Q

what did edward c tolman 1948 discover

A

first to suggest that rodent and humans have a cgonitive map of familiar enviornments
contemporary learning theory accounts held that navigation was completed by rule learning

174
Q

during active navigation which brain area in rats showed inreased activation

A

right hippocampus

175
Q

does the structure of the hippocampus change with navigational experience / expertise

A

maguire et al 2006
posterior hippocampus size in humans is larger in london taxi drivers than control subjects
posterior hippocampus volume correlates with years of taxi driving experience
increase not seen in bus drivers

176
Q

how can spatial and navigational memory be tested in rats

A

the morris watermaze - big pool of water with a submerged platform the rats cant see
first rats swims till he finds the platform
pretty quickly rat learns to swim straight to the platform

177
Q

hippocampal damage imparis what in rats

also how does this relate to experiment

A

spatial memory
the rats do learn where the platform is
just start slow and never get as good as control rats
they learn a rule eg go 20cm from wall and swim in a circke until they can find the platform

178
Q

how does the brain make sure we don’t get lost

A

neurons in rat hippocampus fier when the rat is in a specific location = place cells
we know this from single cell recording
so map of your environment

179
Q

are place cells responsible for spatial memory, navigation or both

A

each place cell recieves two different inputs
1 environment
2 navigtional system (grid cells?)

180
Q

what are the inputs to hippocampus

A

medial entorhinal cortex (MEC) and lateral entrohinal cortex (LEC) feed into hippocampus (place cells)

181
Q

is there spatial firing in medial entorhinal cortex (MEC)

A

not compared to place cells who fire in such a specific place
but in grid cells in MEC there are bursts of activity in lots of different places - if you look at these places they form a hexagonal grid
so one single cell can calculate perfect geometry + knows where rat is

182
Q

arguments against spatial firing in medial entorhinal cortex

A

data is just correlational
lesions of dorsolateral band of the MEC were most grid cells does produce spatial maemory and navigational deficits but they didnt just remove grid cells, other cells were removed too

183
Q

directional coding in medial entrohinal cortex

A

fired depending on direction rat head is facing
one cel fired when always facing the same direction
compass + sense of heading

184
Q

what are the spatial memory and navigation systems

A

head direction cells tell us which way we are facing
grid cells tell us how far we have travelled and speed we have travelled - path integration
place cells keep the mao stable by providing landmarks
the hippocampal network keeps track of spatial location relative to landmarks - allocentric memory

185
Q

schizophrenia

background

A

1% of pop will experience at least one major schizophrenic episode in their life
positive and negative cognitive symptoms
men and women equally affected but onset usually slightly later for women
early onset
twin studies show there is a genetic component

186
Q

who first described schizophrenia and how did they describe it

A

Kraeplin 1887
dementia paradox
bleuler first used term schizophrenia and recognised positive and negative symptoms

187
Q

history of treatment of schizophrenia

A

up to 1950s - insulin coma, frontal lobotomy or shock therapy
1952 - laborit discovers first drug therapy - dopamine antagonist

188
Q

what is the dopamine hypothesis

A 
D2 and D3 receptor antagonist greatly reduce the positive symptoms
dopamine agonists (cocaine, amphetamine, L-DOPA etc) can produce psychotic symptoms of schizophrenia
so is dopaminergic activity increased in schizophrenic patients
189
Q

what did Laruelle et al 1996 discover in relation to the dopamine hypothesis

A

dopamine release in striatum in response to amphetamine greater in schizophrenics

190
Q

brain abnormalitites in schizophrenia

A

ventricles are enlarged
reduced cerebral gray matter
dramatic loss of cortical gray matter in adolesence
hypofrontality (leads to decrease in NMDA and dopamine in prefrontal cortex, explains the dopamine hypothesis)

191
Q

problem for drug therapy of schizophrenics

A

dopamine levels are decreased in the prefrontal cortex
dopamine levels are increase in the midbrain
how can we get dopamine in one area and decrease it in another
= partial agonists

192
Q

what do atypical antischizophrenic drugs do

A

reduce dopamine in nucleus accumbens and increase dopamine in prefrontal cortex
are partial agonists

193
Q

affective disorders

background

A

3% of males + 7% of females effected by depression
bipolar
unipolar
28.8 times more likely to commit suicide
some genetic basis although not a single gene is implicated
gene for the serotnin transporter is likely to be involved

194
Q

what is the thought genetic basis of depression

A

short allels for the serotonin transporter gene increase risk of depression
but
only in individuals who have suffered stressful life event
interaction of genetics and environment

195
Q

brain abnormalities in depression

A

reduced volume of amygdala and subgenual anterior cingulate cortex with one or two short alleles of the serotonin transporter gene
decreased activity in subgenual prefrontal cortex associated with depression
amygdala
-usually processes fear and anger then is reset after fearful stimuli
-this inhibition if less prominent in depressed patients

196
Q

drugs (and theories those drugs are based on ) for affective disorders

A

monamine hypothesis
decreased monaminergic (particularly serotonin and noradrenalin) activity causes depression
many classes of drug that affect monoamine activity helps to alleviate depression
MOIs
tricyclic anti-depressants
specific serotonin reuptake inhiitors
serotonin and noradrenalin reuptake inhibitors
lithium

197
Q

more extreme methods of treating depression

A

depp brain stimulation (subgenual anterior cingulate cortex, vagal nerve)
ECT

198
Q

sleep and affective disorders

A

sleep is affected in depressed people (broken sleep, less REM)
sleep depriation can be used as a treatment

199
Q

why do we study fear

A

adaptive mechanism
long lasting
underlies disorders like anxiety, PTSD, depression
easy to study

200
Q

3 classifications of fear responses

A

behavioural - fight or flight
autonomic - heart rate, blood vessels change to enable behavioural response
hormonal - hormones produced to reinforce the autonomic response (eg adrenalin)

201
Q

how do we study fear

A

fear conditioning in rats

202
Q

fear and the role of the amygdala

experiment in rats

A

lesion of the central and lateral nuclei of the amygdala produced deficits in fear conditioning
(no freezing to tone)
single neurons in the lateral nucleus of the amygdala increase their firing rate to conditioned stimuli following training

203
Q

evidence to show humans are social learners

A

fear response to the CS is seen in subjects with no experience of being shocked but who have observed someone else get shocked when the CS was present
it is also seen when subjects are instructed to expect a shock with the CS

204
Q

brain results in whats activated in humans in response to fearful stimuli

A

left amygdala is activated in response to CS following instruction the CS will be paired with a shock (even when no shock given)
there is also laterality - but probably due to language being involved in the instruction
normal conditioned fear induces bilateral activation

205
Q

3 ways to reduce fear

A

extinction
cognitive regulation
reconsolidation

206
Q

extinction of fear in rats

A

in extinction the association between US and CS is not forgotten
we learn a new association between CS and lack of shock / fear
if new learning is blocked in the amygdala (block LTP using NMDA antagonist) then rats do not show extinction

207
Q

what happens to the amygdala during extinction and how

A

amygdala is inhibited
this inhibiton comes from the ventromedial prefrontal cortex
neurons in this region become active during extinction
this inhibits the fear response produced by the amygdala
electrical stimulation of the vmPRC can speed up extinction

208
Q

how can cognitive regulation reduce fear

A

decreases activation in the amygdala
again is mediated through vmPFC
so works by the same mechanism as extinction
basis for cognitive therapy for emotional disorders

209
Q

how does memory reconsolidation reduce fear

A

can we block memory reconsolidation
LTP required
so we could block LTP by blocking protein synthesis
implications for PTSD
but remember this is permament - memories are removed 0 not inhibited as in extinciton which is useful but could potentially be dangerous

210
Q

what is motor contorl and action selection

A

the brain is capabel of very compex sequences of actions
capable of performing multiple behaviours simultaneously
how does the brain control and coordinate movement

211
Q

how is the primary motor cortex organised and who ofund this out and how did he find this out

A

topographically
penfield
during surgery for epilepsy he stimulated the primary motor cortex to examine which parts of the body are controlled by which parts of the primart motor cortex

212
Q

what is the other system within the brain that controls motor function (if not primary motor cortex)

A

cerebellum
acts in conjunction with primary cortex
cerebellum computed the contributions of muscles to perform movements
cerebellum projects via the ventrolateral thalamus back to the motor cortex which allows current movements to be modified

213
Q

damage to cerebellum causes movement effects. what problem is caused by
floccilonodular or vermis damage

A

postural and balance problems

214
Q

damage to cerebellum causes movement effects. what problem is caused by
intermediate zone damage

A

limb rigidity

215
Q

damage to cerebellum causes movement effects. what problem is caused by
lateral zone damage

A

weakness and decomposition of movemnt

216
Q

damage to cerebellum causes movement effects. what problem is caused by
general cerebelum damage

A

cerebellar ataxia (lack of coordination)

217
Q

how doe we plan and execute sequences of movement

A

premotor cortex and supplementary motor area involved in motor planning (SMA)

218
Q

SMA is critical for….

A

learned sequences
lesions impair these
disrupts ability to make a sequence of 3 movements

219
Q

how are actions encoded in the brain

A

mirror neurons
in the ventral premotor cortex and the inferior temporal lobe
respond to the sight of someone else performing a particular movement

220
Q

research into mirror neurons in humans

A

hard to study as in humans not all neurons int he ventrolateral premotor cortes are mirror neurons
emerging evidence = increased activity in the ventral premotor cortex during execution and observation of actions
this area is often called the inferior frontal gyrus

221
Q

when are mirror neurons most active

A

for well practiced beahviours eg playing the piano

222
Q

what is the function of mirror neurons

A

imitation
mechanism for understadnign the actions of others
encode intention

223
Q

mirror neurons in autistic children

A

autistic children have lower activity in the ventral premotor cortex when imitating facial expression compared to controls
the level of activity in the ventral premotor cortex during the task correlates with the symptom of severity
suggested mirror neurons enable us to process and understnad the actions and intentions of others
this anility underlies theory of mind
lack of mirror neuron activity could lead to autism

224
Q

ways to have disorders of movement

A 
cerebellar damage
neurodegerative disorders
damage to the cortical otor areas
-apraxia
-relates to deficits of skilled learned movements
225
Q

what is limb apraxia

A

inappropriate limb movements especially to verbal commands
caused by damage to the left frontal / parietal cortex
often there are lesions to this area
lesions here also produce deficits in ability to comprehend gestures made by others
consistent with mirror neurons processing action / intention info

226
Q

what is constructional apraxia

A

inability to percieve and imagine geometric relations

caused by damage to the right parietla cortex

227
Q

key terms defining consciousness

A

internal knowledge
awareness of thought feeling and volition of the external world
sense of self
condition of waking life

228
Q

sperling 1960 conscious experiment

A

letter grid for 500msec
letters disappeared and asked to recall
typically could recall 4
can also be paired with tones
tone comes as grid is disappearing but subjects will be able to recall all from that top line
so suggests subjects have conscious access to all the letters?

229
Q

access overflow theory - ned block

A

perceptual consciousness has a higher capacity than cognitive access
the fact that when we are cued we can report all of the letters suggests that we are conscious of all of them
the mechanism that allows us to access this information have a limited caacity so we cannot recall all of the items even though we do consciously perceive them

230
Q

what does access overflow theory suggest about consciouss

A

we have two forms of conscious
phenonmenal consciousness - creates a rich dertail perception of everythig]ng we see
access consciousness - information that we can access theough cognitive processez

231
Q

what is inattentional blindness

A

we miss the gorilla in the ball throuwing counting video
not all information from visual experience is perceived
this argues against phenomenal consciousness

232
Q

what is change blindness

A

details no in attentional focus are not consciously perceived
this is not consistent with phenomenal conscious
suggests that obviously different items are consciously processed but subtly different items are not consciously processed

233
Q

the two problems of studying consciousness

A

easy problem
-understanding the mechanisms of supporting cognitive functinos such as language and attention and working memory
hard problem
-what is it like to be conscious
-how does phenonmenal experience arise from physical events in the brain

234
Q

is it possible to study phenomenal consciouss in isolation of cognitive processes

A

daniel dennet - no
is beyond science
sonsciouss cannot be studied without using the set of cognitive capabilities that can access it
can neuroscience shed light on this?

235
Q

is conscious something separate from the brain

what are the different ideas

A 
yes
-mind vs brain
-dualism
-religion
no 
-reductionism (an extension of materialsim) = where most neuroscientists would sit
maybe 
-emergent properties
236
Q

what is the neurobiological basis of consciousness

A

blind sight

recurrent processing

237
Q

blind sight

A

split brain patients (often split by severing the corpus callosum in patients with severe epilepsy)
split brain patients can often identify stimulus that they have previously encountered even though they have no conscious recollection of experiencing it

238
Q

recurrent processing

A

what rather than where is conscious
are there neural mechanisms which support consciousness
visual information is processed very quickly by the visual cortex but this is sub-concsiocus
recurrent processing in the visual pathway conbined with recurrent processinf in the frontal-parietal regions results in conscious perception
so i recurrent processin consciouss?

239
Q

are patients who cannot use language conscious

A

persisten vegetative state
patients who have come orund form a coma but show no awareness
eg 23 year old woman who had a traffic accident had preserved sleep cycles but was unresponsive to external stimuli = is she unconscious or locked in?

240
Q

what do some patients in a persistent vegetative state do to communicate

A

imagine thing
imagining playing tennis = SMA activation
imagining spatial scenes (eg your house ) produces activation in spatial memory system - PPA
so set one as yes and other no
shows still has conscious even though she cant use language
however she still needs attention and working memory to produce this response
doesnt address whether conscious can be studied in isolation of cognition

PS2001 (4 decks)

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