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Biopsych - Neurodevelopmental Disorders + Schizophrenia (+ other mental…

- - - - Genetics is a partial explanation - 85% of individuals with schizophrenia have no first degree relatives with the illness
        
        Gene-environment interactions - environmental factors can affect gene expression, and genes make a person more vulnerable to develop the disease when exposed to certain environmental factors
        -> Study - adopted children with a biological schizophrenic mother but no schizophrenia in adoptive family had a higher probability for developing schizophrenia but the effect is magnified if family is still dysfunctional (Tiernari)
      - Expression of schizophrenia-related genes is associated with multiple aspects of brain development, myelination, transmission of glutaminergic and GABAergic synpases and changes in dopaminergic neuron physiology
        
        Some genes increase the suspectibility to schizophrenia as wel as other psychiatric and neurological disorders
        
        Socioeconomic factors, maternal stress, prenatal infections, urban birth or residing area, birth complications - environmental factors implicated in development of schizophrenia
        
        These early experiences alter typical courses of neurodevelopment leading to schizophrenia in individuals who have genetic susceptibility through epigenetic mechanisms
        
        Autism and schizophrenia share many of the same genetic causal factors and that those who have schizophrenia parents are more likely to have schizophrenia themselves
        
        DNA methylation and histone modifications have been implicated in gene expression for synapse specific proteins in PFC neurons - gene expression can be increased or decreased
        
        Transgenerational epigenetic mechanisms in schizophrenia are of great interest
  - - - Effective drugs have a high dopamine affinity (Snyder et al, 1975)
        
        Haloperidol is an example of an exception to this rule - this is likely due to dopamine binding to more than one dopamine receptor subtype (5 in total)
        
        Chlorpromazine and other antipsychotic drugs in same chemical class (phenothiazines) all bind effectively to both D1 and D2 receptors whereas haloperidol and others in the butyrophenones family all bind effectively to D2 receptors but not D1 receptors
        
        Dopamine theory revised - schizophrenia is caused by hyperactivity specifically at D2 receptors rather than dopamine in general; therefore, typical antipsychotics which bind to these are highly effective in suppressing schizophrenic symptoms
        
        However, the D2 version cannot explain all findings
        
        Although typical antipsychotics block D2 receptor activity, their effects are not apparent for a few weeks
        
        Almost all antipsychotics are only effective in treating positive symptoms
      - Execessive D2 activity is one factor in the disorder - mesocortioclimbic pathway
        
        Atypical antipychotics - effective without binding strongly to D2 receptors, but also has affinity for D1, D4, serotonin and histamine receptors
        
        Renewal of interest in hallucinogenic drugs - using psychdelic drugs to model disorders and has increased understanding of the impacts of drugs on the human rain and the mechanisms of psychedelic drug action
        
        Three important conclusions - psychedelic effects of classical hallucinogens, mimic positive symptoms of schizophrenia by acting as an agnoist of the serotonin type-2a receptor
        
        Antagonists of the serotonin type 2a are effective antipsychotics
        
        Dissociative hallucinogens mimic the negative symptoms of schizophrenia by acting as antagonists of glutamate receptors