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10 Cards in this Set
- Front
- Back
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2 general familial risk factors
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1. Increased Paternal Age
2. Offspring of dual mating or monozygotic twins |
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4 candidate genes
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1. DISC1
2. dysbindin 3. neuregulin 4. COMT |
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DISC1
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-mismigration of cortical neurons
-dysfunctional post synaptic signalling |
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Dysbindin
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-low dysbindin in hippocampus of schizophrenics
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Neuregulin
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-no reduction in startling response; normalized by antipsychotic
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COMT
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-valine variant 4X more active in dopamine metabolism; affects PFC function
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Neurodevelopmental Hypothesis
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1. Primary lesion in PFC
2. PFC normally comes "on-line" in adolescence. 3. PFC defect manifests as negative symptoms 3. PFC defect causes excessive mesolimbic activity. 4. Excess limbic dopamine activity produces positive symptoms 5. Abberant limbic activity may engender sensitization and neurotoxicity |
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Dopamine Hypothesis
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1. D2 receptor affinity correlates with antipsychotic efficay
2. Psychostimulants mimic positive psychotic symptoms |
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Glutamate Hypothesis
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1. NMDA antagonists (PCP, ketamine) mimic both positive and negative symptoms
2. Interneuron NMDA blockade leads to pyramidal glutamtergic hyperactivity 3. Glutamergic hyperactivity leads to neurotoxic and neuroplastic effects and a hyperdopaminergic state |
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NMDA-R1 Hypomorphs
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1. similiar locomotion and stereotypy abnormalities to schizophrenia
2. PCP has no effect 3. Antipsychotics ameliorate the abnormalities |
