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brain and behaviour > lecture 7 - The biological basis of psychological abnormality > Flashcards

lecture 7 - The biological basis of psychological abnormality Flashcards

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The Brain flashcards
1
Q

what are the two types of synapses?

A

electrical synapse and chemical synapse.

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2
Q

what is the function of a synapse?

A

communication between nerve cells- how neurons communicate.

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3
Q

what is an electrical synapse?

A

very small gap between 2 neurons (2-4nm) that allows a very fast transmission from one neurone to the next - ions move directly from one cell to the other.

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4
Q

what is a chemical synapse?

A

larger gap (20-40nm) that allows synaptic communication mediated by the physical movement of chemicals (neurotransmitter).

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5
Q

which is faster chemical synapse or electrical synapse?

A

Electrical.

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6
Q

what separates the neurons by a small gap in chemical synapses?

A

Synaptic cleft.

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7
Q

what arrives at the presynaptic membrane to allow Ca2+ channels to open and fuse into the cell? (chemical synapse)

A

Action potential.

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8
Q

synaptic vesicles fuse with membrane releasing what into the synaptic cleft? (chemical synapse)

A

neurotransmitter.

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9
Q

once the transmitter has binded to the postsynaptic receptors, the receptor changes shape, what channels open? (chemical synapse)

A

ion channels.

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10
Q

if the channel is for Na+ what happens? (chemical synapse)

A

DEPOLARISATION = Excitatory Postsynaptic Potential (EPSP).

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11
Q

if the channel is for Cl- what happens? (chemical synapse)

A

HYPERPOLARISATION= Inhibitory Postsynaptic Potential (IPSP).

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12
Q

what is propogated along the membrane during chemical synapse?

A

EPSP/IPSP.

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13
Q

what are the two types of postsynaptic receptors?

A
  1. Ionotropic receptors - control ion channel directly (fast)
  2. Metabotrophic receptors - causes a separate ion channel to open using G-protein coupling (slower).
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14
Q

what principle do receptors work on?

A

Lock-and-key

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15
Q

what are Ionotropic receptors also known as?

A

Ligand-gated ion channels

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16
Q

where do EPSPs and IPSPs spread towards?

A

The Axon Hillock.

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17
Q

what is the axon hillock?

A

region where the axon leaves the cell body, it is a membrane rich in voltage-gated channels which can initiate APs.

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18
Q

what is spatial summation?

A

many axons converge on one neuron.

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19
Q

what is temporal summation?

A

many EPSPs/IPSPs occur at the same time.

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20
Q

if the sum of EPSPs + IPSPs is below the threshold of -40mV what will happen?

A

Nothing- No AP is generated.

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21
Q

if the sum of EPSPs + IPSPs has reached the threshold of -40mV what will happen?

A

AP elicited, AP travels along the axon to the axon terminal and the AP causes the release of neurotransmitter. PASSING ON the signal to the next postsynaptic neuron.

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22
Q

what can neurotransmitters be ? (2 things)

A

Exitatory OR Inhibitory

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23
Q

what are the 4 main types of neurotransmitters?

A

Monoamines, Amino acids, Catecholamines and Neuropeptides.

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24
Q

name 3 ways in which changes at synapses underly many psychological disorders. (physical and functional change).

A
  1. change in receptor numbers.
  2. change in amount of neurotransmitter released.
  3. change in structure of synapse.
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25
Q

if neurotransmitter was left in the cleft it would lead to persistent EPSP/IPSPs - how is this avoided? (2 ways)

A
  1. NTs moved BACK into the pre-synaptic/other cells by transporters.
    OR
  2. degraded/neutralised by enzymes.
26
Q

what treats depression?

A

SSRIs - Selective Serotonin Reuptake Inhibitors. as depression is due to a lack of Serotonin (NT).

27
Q

what is an example of an SSRI?

A

Prozac- increases the amount of serotonin that can bind to postsynaptic receptors.

28
Q

there are 6 ways in which drugs affect synapses, name them.

A
  1. increasing the no. of APs.
  2. release transmitters from vesicles without impulses.
  3. Blocking re-uptake.
  4. Blocking receptors.
  5. producing more transmitter.
  6. preventing transmitter release.
29
Q

what is unipolar depression?

A

depression that alternates with ‘normal’ emotional states.

30
Q

what is bipolar depression?

A

fluctuation between depressive periods and episodes of euphoric positive mania. (less common than unipolar).
antidepressants have v little effect- Lithium used in the past.

31
Q

Are there higher rates of depression in biological or adoptive parents?

A

Biological.

32
Q

what was the first anti depressants?

A

Monoamine Oxidase Inhibitors (MAOIs) - highly effective but nasty side effects.

33
Q

how do MAIOs work?

A

inhibit an enzyme called monoamine oxidase.
Monoamine oxidase breaks down norepinephrine, serotonin, and dopamine.
When monoamine oxidase is inhibited, norepinephrine, serotonin, and dopamine are not broken down, increasing the concentration of all three neurotransmitters in the brain. Therefore there is more serotonin than before.

34
Q

what are Tricyclic antidepressants? how do they work

A

inhibit re-uptake of neurotransmitters (acrtlycholine) again leaving more to bind with receptors.
Increasing levels of norepinephrine and serotonin, and block the action of acetylcholine.

35
Q

what NTs are part of Catecholamines?

A

Noradrenaline and Dopamine

36
Q

what cant Catecholamines explain and why?

A

depression - because reduced levels of Noradrenaline and dopamine are NOT found. ignores serotonin.

37
Q

what are the problems with the SSRI model?

A

SSRI can increase serotonin levels in hrs- but relief from depression usually takes weeks as observed.
so possibly SSRI effect is via an intermediary response in the brain ? to the increased levels of serotonin.

38
Q

what is serotonin also known as ?

A

5HT.

39
Q

what did Fournier et al discover?

A

compared P’s with a placebo drug and P’s who were taking SSRIs and compared how happier people felt.
results showed that P’s with placebo reported same level of mood with p’s taking SSRIs.
only shows a real effect in extreme cases of depression.

40
Q

What did Drevets (1998) functional neuroimaging on studies of depression show?

A

differences in the prefrontal cortex.

41
Q

what did Andresan (1991) class as positive symptoms (gained behaviour)? For Schizophrenia

A

Halucinations, delusions, bizzare behaviours, disordered thought.

42
Q

what did Andresan (1991) class as negative symptoms (lost behaviour)? For Schizophrenia

A

social withdrawal, blunted emotional response, reduced motivation, poor focus on tasks.

43
Q

Gottesman (1991) did family studies on Schizophrenia what did he conclude?

A

closer biological relatedness - greater chance that the relative will also be schizophrenic.

44
Q

what genes are involved in schizophrenia?

A

neuregluin 1- involved in glutamate, GABA and ACh receptor regulation.
Catecholamine production.

45
Q

what do twin studies show about schizophrenia?

A

twin with schizophrenia wieghs less at birth (diff development in the womb) more psychological distress.

46
Q

what brain abnormalities does schizophrenia show?

A

ventricular abnormalities- however also seen in people with no disorder

47
Q

what brain abnormalities apart from ventricular abnormalities does schizophrenia show?

A

grey matter loss -
shrinkage in the cerebellar vermis,
a thicker corpus callosum
and frontal abnormalities.

48
Q

what did Thompson et al (2001) reveal in early onset schzophrenia?

A

grey matter loss in adolescent brains.

49
Q

how is the hippocampus affected in schizophrenic patients?

A

cellular disorganisation. the most impaired individuals show the greatest disorganisation.
(Conrad, 1991).

50
Q

what is the hypofrontality hypothesis?

A

less activity in frontal lobes in schizophrenics.

51
Q

what did Holmes et al (2005) give evidence for related to the Hypofrontality hypothesis?

A

decreased activity in the right middle frontal gyrus during a context processing task in p’s with schizophrenia.

52
Q

what did Holcomb et (2000) show about Hypofrontality in schizophrenics?

A

they have decreased cerebral blood flow in the anterior cingulate cortex (ACC) during an auditory discrimination task

53
Q

what is the dopamine hypothesis?

A

large doses of amphetamine (strong dopamine agonist) can cause psychosis - similar symptoms to schizophrenia.

54
Q

what are the limitations to the dopamine hypothesis?

A
  • too simplistic
  • some patients show no improvements when treated with a dopamine antagonist
  • clozapine can also increase the levels of dopamine in the frontal cortex.
55
Q

what is the Glutamate hypothesis??

A

glutamate receptor agonist reported to improve +ve and -ve symptoms in schizophrenia.
in schizophrenics glutamate receptors are blocked. PCP blocks it.

56
Q

Anxiety is neccessary as it protects us from dangerous situations when does it become a clinical problem?

A

when it occurs for no reason/ excessively intense/ long lasting.

57
Q

what is panic disorder?

A

overwhelming anxiety, feeling about to die.

58
Q

what are the causes of panic disorder?

A

psychological factors- general stress/life transitions
stimulants
metabolic hypothesis of panic- triggers= lactate and carbon dioxide
temporal lobe abnormalities.

59
Q

what did Zieman et al (2009) say about the amygdala?

A

that it is a chemosensor that reacts to changes in the bodys pH produced by high levels of Co2.

60
Q

what did Hayano et al (2009) say about panic disorder and the amygdala?

A

smaller amygdala is associated with anxiety.

61
Q 
what are the following associated with:
SSRIs
Diazepam
Clozapine
Lithium
TADs
MAOIs
A 
SSRIs – Serotonin,
 Diazepam – GABA, 
Clozapine – Serotonin and dopamine, 
Lithium – Glutamate, 
TADs – Noradrenaline and dopamine,
 MAOIs – Noradrenaline and dopamine

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