Steven Crane Compiled Section Handouts. Human Behavioral Biology 2012

Clinical finding
Cause of enhanced dopamine signaling
Low breakdown product	COMT enzyme is broken
Normal breakdown product	Just too many or too sensitive of receptors for dopamine
High breakdown product	Too much dopamine released

What's the neurological logic connecting dopamine to schizophrenia symptoms?

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  Unclear, but probably not about pleasure/anticipation.
  
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  Probably something with mesolimbic dopamine projections into the frontal cortex, somehow disrupting executive function and logical, sequentially ordered thought
  

What's the evidence implicating serotonin in schizophrenia?

• Hallucinogenic drugs (LSD/acid, mescaline, and psilocybin/magic mushrooms) are basically exogenous serotonin and they cause hallucinations just like in schizophrenia.

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  Blocking a serotonin receptor relieves some of the negative symptoms of schizophrenia
  

And the evidence implicating glutamate? (Not a whole lot)

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  Drug called phencyclidine (PCP/angel dust) can produce a psychotic state similar to schizophrenia and it works on glutamate pathways.
  
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  Preadolescent children (who can't get schizophrenia) also can't be made psychotic by PCP. I'd like to see the informed consent for that experiment...
  

What are the structural and cellular differences in the brain in schizophrenia?

Why is it hard to even get answers to these questions?

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  You often need VERY recently alive brains to cut up, stain, etc. to measure brain and cellular structures. Hard to get. When you take brains out you squish them too.
  
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  Other problem: schizophrenics often have poor nutrition, vitamin deficiencies, and also take tons of drugs to treat their condition. So you don't know if your findings are due to the actual brain abnormalities that caused schizophrenia or those other confounds
  

How can you get around those issues?

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