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Brain and Behaviour > Cognition and Reward > Flashcards

Cognition and Reward Flashcards

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1
Q

What are positive symptoms?

A

distorted or excess of normal functioning

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2
Q

What are positive symptoms of Schizophrenia?

A

delusions, hallucinations and thought disorders

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3
Q

What are negative symptoms?

A

deficit or decrease in normal functioning

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4
Q

What are negative symptoms of Schizophrenia?

A

flattened emotional response, poverty of speech, social withdrawal and anhedonia

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5
Q

What is the early neurodevelopment model of Schizophrenia?

A

during the second trimester lesions appear which lie dormant until the brain matures and required these areas (Murray and Lewis 1987)

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6
Q

What is the late neurodevelopment model of Schizophrenia?

A

an abnormality in peri-adolescent synaptic pruning (Feinberg 1983)

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7
Q

What is the 2 hit model of Schizophrenia?

A

the combination of both early and late developmental problems

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8
Q

What physical brain change is observed in Schizophrenia?

A

ventricular enlargement, loss of grey matter reduced temporal, frontal and subcortical matter

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9
Q

What is hypofrontality?

A

a decrease in blood flow to the prefrontal cortex (mesocortical area) leading to decreased brain activity during high cognitive load

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10
Q

What neurocognitive deficits are observed in Schizophrenia?

A

lower IQ, attentional deficit, working memory deficit, planning and information processing deficit, lack of filtering out irrelevant information

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11
Q

What neurophysiological deficits are observed in Schizophrenia?

A

pre-pulse inhibition and oculomotor functions

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12
Q

What is pre-pulse inhibition?

A

schizophrenics are unable to inhibit a startle response despite being given a preceding stimulus

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13
Q

What are oculomotor functions?

A

tracking a spot smoothly and suppression of looking at a target

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14
Q

What does the mesolimbic system consist of?

A

ventral tegmentum and nucleus accumbens

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15
Q

How is the mesolimbic system related to Schizophrenia?

A

an overactive mesolimbic system (increased dopamine) leads to positive symptoms

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16
Q

How is the mesocortical system related to Schizophrenia?

A

reduced activity in the mesocortical (reduced dopamine) leads to negative symptoms

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17
Q

What does the mesocortical system consist of?

A

ventral tegmentum and prefrontal cortex

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18
Q

What is some evidence for the role of dopamine in Schizophrenia?

A

effectiveness of dopamine antagonists, drugs boosting dopamine can induce positive symptoms, increased dopamine in caudate putamen

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19
Q

What are some problems with the dopamine hypothesis?

A

only explains positive symptoms, dopamine antagonists exacerbate negative symptoms

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20
Q

What is the glutamate hypofunctioning theory?

A

positive symptoms in Schizophrenia such as delusions and hallucinations are the result of decreased glutamate

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21
Q

What evidence is there for glutamate hypofunctioning theory?

A

NMDA receptor antagonists (ketamine) can induce hypo function and glutamate agonists improve both positive and negative symptoms

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22
Q

How does glutamate affect dopamine?

A

glutamate excites GABA which then causes the inhibition of dopamine

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23
Q

How can glutamate affect neurodevelopment?

A

excitotoxicity can cause problems with neural pathways, migration, plasticity and pruning

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24
Q

What can glutamate excitotoxicity lead to in later life?

A

glutamate hypofunctioning

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25
Q

What is apoptosis?

A

programmed cell death caused by neurostructural changes

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26
Q

How is microglial activity related to Schizophrenia?

A

brain immune cells are hyperactive in people at risk of developing the disease

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27
Q

What evidence is there for the role of microglial activity in Schizophrenia?

A

blocking/reducing microglial activation in premorbid schizophrenics may alleviate some symptoms

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28
Q

What has genome analysis revealed about the causes of Schizophrenia?

A

dopamine receptor gene is associated with risk of Schizophrenia, more than 100 loci associated with Schizophrenia risk

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29
Q

What is major depressive disorder?

A

more intense and longer lasting feelings of sadness - 3x more likely in females than males

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30
Q

What is affective disorder?

A

extreme of inappropriate exaggeration of mood

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31
Q

What is bipolar disorder?

A

bouts of depression or mania

32
Q

What evidence is there for the role of genetics in mood disorders?

A

relatives of those with a mood disorder are 2 to 3 times more likely to have one, if an identical twin has a mood disorder the other twin is 3x more likely to have one

33
Q

What are some symptoms of major depression?

A

depressed mood, anhedonia, weight loss/gain, insomnia/hypersomnia, psychomotor agitation/retardation

34
Q

How is serotonin, dopamine and norepinephrine linked to depression?

A

lowered levels of these metabolites are in the CSF of depressed individuals

35
Q

How can Reserpine induce depressive symptoms?

A

it blocks the packaging of monoamines into the vesicles so no transmitter can be released

36
Q

How is Tryptophan involved in depression?

A

patients on a tryptophan free diet had a 50% depletion of serotonin causing depressive symptoms to reoccur

37
Q

What evidence is there for the role of serotonin in depression?

A

anti-depressant medications work by changing serotonin levels, suicidal patients are characterised as having particularly low levels of serotonin

38
Q

What are the types of antidepressant medications?

A

monoamine oxidase inhibitors, monoamine reuptake inhibitors and selective serotonin reuptake inhibitors

39
Q

How do monoamine oxidase inhibitors work?

A

inhibits the amine which breaks down monoamines in the synaptic cleft

40
Q

How do monoamine reuptake inhibitors work?

A

prevent the reuptake of monoamines into the synaptic terminal

41
Q

How do selective reuptake serotonin inhibitors work?

A

block the breakdown (increased pool) of monoamines and blocks the reuptake (increased signal) of monoamines

42
Q

What physical changes are seen in the brain with depression?

A

reduced hippocampal volume

43
Q

What is the HPA axis?

A

Hypothalamus releases CRH
Pituitary gland releases ACTH
Adrenal gland released cortisol

44
Q

How can chronic stress induce depression?

A

chronic stress can cause chronic activation of glucocorticoid receptors, too much Ca2+ entry can cause excitotoxicity and cell death; hippocampus cannot feedback

45
Q

How are depressed patients more at risk of stress?

A

the stress activation system is very sensitive, they have high blood levels of cortisol, high brain levels of CRH and fewer glucocorticoid receptors

46
Q

What are some genetic risk factors associated with depression?

A

a mutation in he serotonin transporter gene was found to moderate the influence of stressful life events and individuals with one or two short alleles of the 5-HTT premotor polymorphism exhibit more depressive symptoms

47
Q

Why is the therapeutic effect so slow?

A

increase in CREB is slow, brain growth and receptor regeneration due to BDNF is slow

48
Q

What is tolerance?

A

the diminishing effect of a drug so more is required for the same effect (homeostatic-compensatory change)

49
Q

What is dependence?

A

physical or adaptive changes, a homeostatic response to repeated administration, can lead to withdrawal (homeostatic-compensatory change)

50
Q

What is sensitisation?

A

repeated administration elicits escalating effects e.g. psychostimulants (associative learning)

51
Q

How do amphetamines directly induce reward?

A

increase the availability of dopamine at the synapse by blocking or reversing reuptake

52
Q

How does nicotine directly induce reward?

A

direct excitation of VTA neurons by actions at nicotinic receptors

53
Q

How do opioid and cannabinoids indirectly induce reward?

A

action at opioid or cannabinoid receptors indirectly leads to modulation of VTA activity

54
Q

What happens during associative learning?

A

NAcc firing coincident with a reward associated cue will induce LTP strengthening synaptic connections

55
Q

How does dopamine affect LTP?

A

glutamatergic transmission is modified, synaptic remodelling, long term molecular changes, pathway memory can trigger relapse

56
Q

What physical change can be caused by chronic substance abuse?

A

frontal lobe dysfunction - hypoactivity

57
Q

How can hypoactivity explain addictive behaviour?

A

loss of motivational control of drug seeking behaviour and loss of inhibitory control to resist drugs when exposed to them

58
Q

What evidence is there for the mesocorticolimbic pathway in addiction?

A

damage to the NAcc decreases heroin self administration and drugs of abuse maintain dopamine release in NAcc after repeated exposure

59
Q

How do opiates have a rewarding effect?

A

they act at endogenous opioid receptors decreasing adenylyl cyclase activity, act as an analgesic at the mu receptors

60
Q

How does alcohol affect brain functioning?

A

inhibits the functioning of most channels, prevents NMDA excitation

61
Q

How does alcohol induce reward?

A

increased dopamine release in the NAcc;

1) Supression of cortical output
2) No activation of GABA interneuron
3) DA neurons are disinhibited in VTA and become able to fire

62
Q

How does nicotine induce reward?

A

increased dopamine release in the NAcc due to activation of nicotinic ACh and facilitation of dopamine release by pre-synaptic receptors in NAcc

63
Q

How does opiate dependence occur?

A

chronic activation of opiate receptors leads to homeostatic mechanism which compensates for the functional changes, leading to dependence

64
Q

What are the effects of acute morphine dependence?

A

acute inhibition of firing of locus coeruleus neurons through Gi pathway

65
Q

What are the effects of chronic morphine dependence?

A

locus coeruleus neurons return to normal firing rate (Gs pathway upregulates to match Gi)

66
Q

What are the effects of withdrawal?

A

dramatic increase in locus coeruleus firing (in absence of Gi inhibition Gs hypersensitive)

67
Q

What are the acute effects of alcohol?

A

agonist at GABA receptor and antagonist at NDMA receptor; cells are inhibited from firing

68
Q

What are the chronic effects of alcohol?

A

down-regulation of GABA receptors and up-regulation of NMDA receptors; in the presence of alcohol, firing rates return to normal

69
Q

What effect does alcohol withdrawal have?

A

in the absence of alcohol the balance shifts to excitation and physical symptoms

70
Q

What effect on control functions does the addicted brain show?

A

weakening of top-town inhibitory control functions and strengthening of bottom-up functions

71
Q

What are the 3 main subtypes of behavioural impulsivity?

A

temporal, motor inhibition and reflection

72
Q

Describe the temporal impulsive subtype and how it is tested

A

inability to delay gratification; tested with a delay discounting task

73
Q

Describe the motor inhibition impulsive subtype and how it is tested

A

inability to inhibit responding; tested with a GO/ NO GO or stop signal test

74
Q

Describe the reflection impulsivity subtype and how it is tested

A

inability to reflect before making a decision; tested by a matching familiar figures test

75
Q

What are the main causes of impulsivity?

A

neglect and trauma

76
Q

What are some physical features of a brain of an individual with ADHD?

A

smaller prefrontal cortex and cerebellum, delayed cortical thinning, reduced signalling in reward pathways

Brain and Behaviour (9 decks)

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