biological explanation - the dopamine hypothesis Flashcards

1
Q

when a nerve impulse travels to the pre-synaptic terminal, what does the pre-synaptic terminal release?

A

neurotransmitters

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2
Q

what do these neurotransmitters bind to and what does it allow?

A

the post synaptic receptors allowing positively or negatively charged particles into the post-synaptic neuron.

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3
Q

the ….. excitatory neurotransmitters that bind to post synaptic receptors, the more ….. charged particles flow into the post-synaptic neuron and the more EPSPs are generated.

A

the more excitatory neurotransmitters that bind to post synaptic receptors, the more positively charged particles flow into the post-synaptic neuron and the more EPSPs are generated

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4
Q

what is dopamine and what is it involved in?

A

dopamine is a neurotransmitter. dopamine is involved in processing reward and in controlling attention.

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5
Q

according to the dopamine hypothesis of schizophrenia, people with schizophrenia have what and where does this occur?

A

higher levels of dopamine than normal. these high levels don’t occur all over the brain. they just occur in a group of brain regions which is collectively called the mesolimbic system.

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6
Q

in the mesolimbic system, is dopamine excitatory or inhibitory and how does this cause over activity in the mesolimbic system?

A

dopamine has an excitatory effect meaning that if their are higher levels of dopamine, neurons generate more electrical activity than normal. this causes over activity in the mesolimbic system.

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7
Q

according to the dopamine hypothesis of schizophrenia, what does this overactivity in the mesolimbic system cause?

A

this overactivity in the mesolimbic system is what causes people with schizophrenia to experience hallucinations and delusions. so, the dopamine hypothesis suggests that schizophrenia is caused by abnormal brain function.

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8
Q

what doesn’t the dopamine hypothesis explain?

A

why people with schizophrenia also have negative symptoms

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9
Q

to explain the negative symptoms of schizophrenia, what did researchers come up with?

A

a revised dopamine hypothesis

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10
Q

what does the revised dopamine hypothesis suggest?

A
  • that there is too much dopamine in the mesolimbic system. these increased levels of dopamine lead to neurons becoming overactive.
  • it also suggests that in other parts of the brain, the levels of dopamine are low. in particular, people with schizophrenia have low levels of dopamine in the frontal cortex. low levels of dopamine cause under activity of neurons in the frontal cortex. since the frontal cortex plays a role in making us feel motivated to achieve our goals, under activity in the frontal cortex causes negative symptoms of schizophrenia like avolition.
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11
Q

support for the dopamine hypothesis - drug studies

A
  • there are some drugs that can increase dopamine activity in the brain for a short period of time. for example, there is a drug called amphetamine which is known to increase dopamine activity.
  • according to the dopamine hypothesis, if a person takes an amphetamine their dopamine activity will increase and so their should be increased activity in the mesolimbic pathway. this leads to hallucinations and delusions.
  • studies have tested this prediction by giving amphetamines to healthy participants. they found that healthy participants experienced hallucinations and delusions just like people with schizophrenia.
  • there are also drugs that decrease dopamine activity. according to the dopamine hypothesis, these drugs should make people with schizophrenia less likely to experience hallucinations and delusions
  • studies have also tested this predication by giving drugs that decrease dopamine activity to people with schizophrenia and these studies have demonstrated that these drugs reduce their positive symptoms.
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12
Q

limitation of the dopamine hypothesis - don’t always prevent positive symptoms

A
  • drugs that decrease dopamine levels don’t always prevent hallucinations and delusions
    -if abnormally high levels of dopamine in the mesolimbic system causes hallucinations and delusions, then we would expect that ALL patients would experience a reduction in positive symptoms. but this isn’t what studies found
  • in 2009, noll reviewed all of the drug studies, in which doctors gave drugs to people with schizophrenia in order to decrease their dopamine levels. noll found that for many patients, decreasing their levels of dopamine did stop patients from experiencing hallucinations and delusions.
  • this suggests that for these patients their positive symptoms were abused by abnormally high levels of dopamine. but for 1/3 of patients the drugs didn’t stop them experiencing hallucinations and delusions. this suggests that for these patients, their positive symptoms weren’t caused by abnormally high dopamine levels in the mesolimbic system. so there may be other causes of positive schizophrenia symptoms as well as having high level of dopamine
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13
Q

limitation of the dopamine hypothesis - evidence supporting isn’t conclusive

A
  • in 2009, moncrieff reviewed the studies investigating the dopamine hypothesis. based on these studies, moncrieff made 2 main criticisms of the dopamine hypothesis.
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14
Q

what was moncreiff’s first criticism of the dopamine hypothesis

A

1) drugs that cause hallucinations and delusions (amphetamines) don’t just increase dopamine activity. these drugs also effect the activity of other neurotransmitters like serotonin and noradrenaline. it is possible that hallucinations and delusions aren’t caused by increased dopamine activity. instead, are caused by increased serotonin or noradrenaline

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15
Q

what was moncrieff’s second criticism of the dopamine hypothesis?

A

2) there is little direct evidence that people with schizophrenia have an imbalance of dopamine activity. moncrieff reviewed the studies that had used post-mortem examinations to look at changes in dopamine levels, in the brains of patients with schizophrenia. according to the dopamine hypothesis, these studies should have found increased levels of dopamine in mesolimbic system in the brain’s of patients with schizophrenia. but what moncrief found was that some post mortem studies reported increased levels of dopamine. however, other studies reported no difference in the levels of dopamine of patients with schizophrenia compared to the control brains.

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