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10 Cards in this Set

  • Front
  • Back
2 general familial risk factors
1. Increased Paternal Age

2. Offspring of dual mating or monozygotic twins
4 candidate genes
1. DISC1
2. dysbindin
3. neuregulin
-mismigration of cortical neurons
-dysfunctional post synaptic signalling
-low dysbindin in hippocampus of schizophrenics
-no reduction in startling response; normalized by antipsychotic
-valine variant 4X more active in dopamine metabolism; affects PFC function
Neurodevelopmental Hypothesis
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
Dopamine Hypothesis
1. D2 receptor affinity correlates with antipsychotic efficay

2. Psychostimulants mimic positive psychotic symptoms
Glutamate Hypothesis
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
NMDA-R1 Hypomorphs
1. similiar locomotion and stereotypy abnormalities to schizophrenia

2. PCP has no effect

3. Antipsychotics ameliorate the abnormalities