schizophrenia: bio explanation - NTs Flashcards

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1
Q

what is a neurotransmitter?

A
  • the body’s chemical messengers
  • molecules used by nervous system to transmit messages between the neurons
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2
Q

what is dopamine?

A
  • neurotransmitter made in your brain
  • plays as a ’reward centre’/sense of pleasure
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3
Q

what is it meant by hyperdopaminergia?

A
  • overactive
  • having too much dopamine activity
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4
Q

what is hypodopaminergia?

A
  • underactive
  • having too little dopamine activity
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5
Q

what is a dopamine agonist?

A
  • drugs that activate certain types of cells in your brain
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6
Q

what is the mesocortical pathway?

A
  • neural connection between ventral tegmental area and the frontal cortex
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7
Q

what is the mesolimbic pathway?

A
  • begins in the ventral tegmental area and connects nucleus accumbens, amygdala, hippocampus and prefrontal cortex
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8
Q

what is glutamate?

A
  • most abundant excitatory neurotransmitter in your brain and central nervous system
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9
Q

what is antagonist?

A
  • chemical/medication that attaches to brain receptors and inhibits an antagonist from reacting
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10
Q

what is amphetamine?

A
  • stimulant drugs that speed up messages between brain and body
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11
Q

what is the dopamine hypothesis?

A
  • states that the brain of schizophrenic patients produces more dopamine than the brain of a “normal person
  • through research, it is now thought that schizophrenics have an abnormally high number of d2 receptors
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12
Q

how can dopamine be linked to schizophrenia?

A
  • dopamine (or da and specifically d2 receptors), a neurotransmitter has been linked to schizophrenia
  • dopamine is present in higher levels in the brain and this leads to symptoms of schizophrenia
  • presence of excess number of dopamine receptors at the synapses in the brain contributes to the illness
  • if there’s an increase in the mesolimbic pathway, then positive symptoms are presented and if there is a decrease in the mesocortical pathway contributes to negative symptoms
  • neurons that use dopamine fire too often and transmit too many messages or too often
  • certain d2 receptors are known to play a key role in guiding attention
  • lowering da activity helps remove the symptoms of schizophrenia
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13
Q

what are the role of drugs linked to schizophrenia?

A
  • amphetamines (agonists) lead to increase in da levels
  • large quantities lead to delusions and hallucinations
  • if drugs are given to schizophrenic patients their symptoms get worse
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14
Q

what is the glutamate hypothesis?

A
  • theory that first emerged in the 1980s, but which has gained wider support, traces the origins of schizophrenia symptoms to the neurotransmitter glutamate rather than dopamine
  • glutamate is the major “excitatory” neurotransmitter in the brain, which means that it helps to activate neurons and other brain cells
  • theory that decreased activity of the excitatory neurotransmitter glutamate is responsible for the clinical expression of schizophrenia
  • developed by overseeing symptoms induced by phencyclidine that act as antagonists at nmda receptors
  • glutamate is thought to control the amount of dopamine released by the brain, and normally seems to lower levels of dopamine
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15
Q

evidence for neurotransmitters as explanation: Falkai et al 1988

A
  • autopsies have found people with schizophrenia have larger than usual number of dopamine receptors
  • increase of da in brain structures and receptor density (left amygdala and caudate nucleus putamen)
  • concluded that da production is abnormal for schizophrenia
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16
Q

evidence for neurotransmitters as explanation: Lindstroem et al 1999

A
  • radioactively labelled chemical called L-DOPA, used by the brain to produce dopamine
  • they ** administered the l-dopa to ten untreated patients** with schizophrenia and a control group of ten people with no diagnosis
  • using pet scans, they were able to trace what happened to the l-dopa
  • l-dopa was taken up more quickly in patients with schizophrenia, suggesting they were producing more dopamine than the control group
17
Q

evidence for neurotransmitters as explanation: Snyder 1985

A
  • found chlorpromazine acts as an antagonist at many dopamine receptors, especially. d1 and d2, and has antipsychotic effect
  • haloperidol is a dopamine antagonist with a narrower range of biochemical effects yet is more effective in reducing schizophrenic symptoms
  • findings suggest that excess activity on specific but not all dopamine receptors is implicated in the development of symptoms
18
Q

evidence for neurotransmitters as explanation: haloperidol

A
  • dopamine antagonists that bond to d2 receptors such as haloperidol, can successfully reduce positive symptoms
19
Q

evidence for neurotransmitters as explanation: Tenn et al 2003

A
  • found that rats given 9 amohetamine injections over 3 weeks showed various schizophrenia like symptoms
  • dopamine antagonists (drugs that dopamine d1 receptors) were successful in reversing these effects
20
Q

strengths: supporting evidence

A
  • Lindstroem et al 1999 found **schizophrenics used L-DOPA faster than the control group, suggesting they were producing more dopamine at a quicker rate, and the **excess dopamine can explain how schizophrenia is caused
21
Q

weaknesses: opposing evidence

A
  • PET scans show that blocking receptors does not always remove symptoms. PET scans have suggested that drugs that block dopamine do not reduce the symptoms of schizophrenia, in particular those who had schizophrenia for 10 years
  • Depatie + Lal 2001 found that giving people drugs that increase production of dopamine does not create symptoms of schizophrenia as would be expected if excess dopamine caused it, so it is **not the only explanation of the causes of schizophrenia (can be different things as well)
22
Q

weaknesses: different things

A
  • anti-psychotic drugs block dopamine receptors very quickly but it takes a few days for the symptoms of schizophrenia to be reduced so there may be other factors involved in developing schizophrenia, not just neurotransmitters so it does not fully explain the development of schizophrenia
  • Wim Veling et al 2008 shows that Moroccan immigrants were more likely to be diagnosed with schizophrenia than Turkish immigrants. This correlated to the amount of actual and perceived discrimination faced by each group. this suggests that environmental factors such as social stress may interact with internal neurochemistry making some people more prone to psychosis
  • neurotransmitter explanation of schizophrenia can be said to be incomplete as it ignores other possible causes of schizophrenia such as early childhood experiences or cognitive processes, and it is not the only explanation. researchers at Liverpool University in 2012 found that childhood trauma makes you three times more likely to develop schizophrenia, suggesting that there is strong relationship between the environment and the development of schizophrenia, and it is not just due to neurotransmitters
23
Q

strengths: other things

A
  • amphetamines produce symptoms similar to those of excess dopamine. this psychosis is called ’amphetamine psychosis’ and the symptoms are similar to those positive symptoms of schizophrenia
24
Q

weaknesses: other things

A
  • using pet scanning to obtain evidence about neurotransmitter functioning could affect validity. when undergoing scanning humans might feel under pressure and are likely to respond differently from normal. this means that any findings gathered might not be accurate