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Brain and Behaviour > Cognition and Reward > Flashcards

Cognition and Reward Flashcards

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
What is apoptosis?
programmed cell death caused by neurostructural changes
26
How is microglial activity related to Schizophrenia?
brain immune cells are hyperactive in people at risk of developing the disease
27
What evidence is there for the role of microglial activity in Schizophrenia?
blocking/reducing microglial activation in premorbid schizophrenics may alleviate some symptoms
28
What has genome analysis revealed about the causes of Schizophrenia?
dopamine receptor gene is associated with risk of Schizophrenia, more than 100 loci associated with Schizophrenia risk
29
What is major depressive disorder?
more intense and longer lasting feelings of sadness - 3x more likely in females than males
30
What is affective disorder?
extreme of inappropriate exaggeration of mood
31
What is bipolar disorder?
bouts of depression or mania
32
What evidence is there for the role of genetics in mood disorders?
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
What are some symptoms of major depression?
depressed mood, anhedonia, weight loss/gain, insomnia/hypersomnia, psychomotor agitation/retardation
34
How is serotonin, dopamine and norepinephrine linked to depression?
lowered levels of these metabolites are in the CSF of depressed individuals
35
How can Reserpine induce depressive symptoms?
it blocks the packaging of monoamines into the vesicles so no transmitter can be released
36
How is Tryptophan involved in depression?
patients on a tryptophan free diet had a 50% depletion of serotonin causing depressive symptoms to reoccur
37
What evidence is there for the role of serotonin in depression?
anti-depressant medications work by changing serotonin levels, suicidal patients are characterised as having particularly low levels of serotonin
38
What are the types of antidepressant medications?
monoamine oxidase inhibitors, monoamine reuptake inhibitors and selective serotonin reuptake inhibitors
39
How do monoamine oxidase inhibitors work?
inhibits the amine which breaks down monoamines in the synaptic cleft
40
How do monoamine reuptake inhibitors work?
prevent the reuptake of monoamines into the synaptic terminal
41
How do selective reuptake serotonin inhibitors work?
block the breakdown (increased pool) of monoamines and blocks the reuptake (increased signal) of monoamines
42
What physical changes are seen in the brain with depression?
reduced hippocampal volume
43
What is the HPA axis?
Hypothalamus releases CRH Pituitary gland releases ACTH Adrenal gland released cortisol
44
How can chronic stress induce depression?
chronic stress can cause chronic activation of glucocorticoid receptors, too much Ca2+ entry can cause excitotoxicity and cell death; hippocampus cannot feedback
45
How are depressed patients more at risk of stress?
the stress activation system is very sensitive, they have high blood levels of cortisol, high brain levels of CRH and fewer glucocorticoid receptors
46
What are some genetic risk factors associated with depression?
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
Why is the therapeutic effect so slow?
increase in CREB is slow, brain growth and receptor regeneration due to BDNF is slow
48
What is tolerance?
the diminishing effect of a drug so more is required for the same effect (homeostatic-compensatory change)
49
What is dependence?
physical or adaptive changes, a homeostatic response to repeated administration, can lead to withdrawal (homeostatic-compensatory change)
50
What is sensitisation?
repeated administration elicits escalating effects e.g. psychostimulants (associative learning)
51
How do amphetamines directly induce reward?
increase the availability of dopamine at the synapse by blocking or reversing reuptake
52
How does nicotine directly induce reward?
direct excitation of VTA neurons by actions at nicotinic receptors
53
How do opioid and cannabinoids indirectly induce reward?
action at opioid or cannabinoid receptors indirectly leads to modulation of VTA activity
54
What happens during associative learning?
NAcc firing coincident with a reward associated cue will induce LTP strengthening synaptic connections
55
How does dopamine affect LTP?
glutamatergic transmission is modified, synaptic remodelling, long term molecular changes, pathway memory can trigger relapse
56
What physical change can be caused by chronic substance abuse?
frontal lobe dysfunction - hypoactivity
57
How can hypoactivity explain addictive behaviour?
loss of motivational control of drug seeking behaviour and loss of inhibitory control to resist drugs when exposed to them
58
What evidence is there for the mesocorticolimbic pathway in addiction?
damage to the NAcc decreases heroin self administration and drugs of abuse maintain dopamine release in NAcc after repeated exposure
59
How do opiates have a rewarding effect?
they act at endogenous opioid receptors decreasing adenylyl cyclase activity, act as an analgesic at the mu receptors
60
How does alcohol affect brain functioning?
inhibits the functioning of most channels, prevents NMDA excitation
61
How does alcohol induce reward?
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
How does nicotine induce reward?
increased dopamine release in the NAcc due to activation of nicotinic ACh and facilitation of dopamine release by pre-synaptic receptors in NAcc
63
How does opiate dependence occur?
chronic activation of opiate receptors leads to homeostatic mechanism which compensates for the functional changes, leading to dependence
64
What are the effects of acute morphine dependence?
acute inhibition of firing of locus coeruleus neurons through Gi pathway
65
What are the effects of chronic morphine dependence?
locus coeruleus neurons return to normal firing rate (Gs pathway upregulates to match Gi)
66
What are the effects of withdrawal?
dramatic increase in locus coeruleus firing (in absence of Gi inhibition Gs hypersensitive)
67
What are the acute effects of alcohol?
agonist at GABA receptor and antagonist at NDMA receptor; cells are inhibited from firing
68
What are the chronic effects of alcohol?
down-regulation of GABA receptors and up-regulation of NMDA receptors; in the presence of alcohol, firing rates return to normal
69
What effect does alcohol withdrawal have?
in the absence of alcohol the balance shifts to excitation and physical symptoms
70
What effect on control functions does the addicted brain show?
weakening of top-town inhibitory control functions and strengthening of bottom-up functions
71
What are the 3 main subtypes of behavioural impulsivity?
temporal, motor inhibition and reflection
72
Describe the temporal impulsive subtype and how it is tested
inability to delay gratification; tested with a delay discounting task
73
Describe the motor inhibition impulsive subtype and how it is tested
inability to inhibit responding; tested with a GO/ NO GO or stop signal test
74
Describe the reflection impulsivity subtype and how it is tested
inability to reflect before making a decision; tested by a matching familiar figures test
75
What are the main causes of impulsivity?
neglect and trauma
76
What are some physical features of a brain of an individual with ADHD?
smaller prefrontal cortex and cerebellum, delayed cortical thinning, reduced signalling in reward pathways

Brain and Behaviour (9 decks)

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