Steven Crane Compiled Section Handouts. Human Behavioral Biology 2012

What is the neurochemistry and brain metabolism of schizophrenia?

What are the three NTs implicated?

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  Dopamine, serotonin, glutamate
  

What's the evidence that schizophrenia is a disease of too much dopamine signaling?

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  First, this could mean that there's too much dopamine NT floating around OR that the post-synaptic neuron is
  

more sensitive to dopamine

1. 
   Antipsychotic drugs like thorazine and haldol decrease schizophrenic symptoms and their mechanism is too block dopamine receptors
   
2. 
   We see a lot of dopamine breakdown products in CSF, blood, urine
   
3. 
   We see more dopamine receptors in some post-mortem studies of schizophrenic brains
   
4. 
   Some studies show that schizophrenics are more responsive to drugs that have dopamine-like actions
   
5. 
   If you treat Parkinson's disease (disease of TOO LITTLE dopamine) with drugs that raise dopamine levels, you get schizophrenia-like side effects. And vice versa (inhibit dopamine signaling to treat schizophrenia and you can get Parkinson's-like symptoms).
   

What's the evidence that schizophrenia is a disease of too little dopamine breakdown?

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  Idea being that dopamine levels are fine, but when they come off the receptor, the COMT enzyme is not working properly, and dopamine is not degraded. Too much is left in the synapse.
  

Complicating our measure of dopamine breakdown product in the urine, how can it be that enhanced dopamine signaling could produce abnormally high, normal, or abnormally low dopamine breakdown product levels in the urine?

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  Too much dopamine signaling in the synapse leads to:
  

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