modifying schizophrenia- antipsychotics

  • Created by: Elyseee
  • Created on: 29-01-21 12:57
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  • antipsychotics
    • Conventional antipsychotics
      • Aka first generation, older, typical - developed in 1950s
      • Chlorpromazine
      • Affects neurotransmission - blocks action of dopamine, acts primarily as antagonist of D2 receptors, also blocks receptors D1-5
      • Presynaptic neuron releases dopamine into synapse, receptor sites are blocked which reduces postsynaptic activity. Initially there is a rise in dopamine secretion. Amount of dopamine drops because it is depleted, amount of dopamine in synapse decreases. Lower levels of dopamine in synapse and blocking by chlorpromazine lead to decreased neural activity
      • Reduction of dopamine activity in mesolimbic pathway thought to be responsible for decreased positive symptoms eg) hallucinations, delusions
      • Chlorpromazine also affects serotonin receptor sites eg) 5-HT1 and 5HT-2, and other receptor sites, but mainly dopamine
    • Atypical antipsychotics
      • Aka newer, second generation - developed since 1990s
      • Clozapine
      • Act as dopamine antagonists
      • Mechanisms are unclear
    • Differences
      • Some report atypical antipsychotics are different from conventional because they are received at fewer D2 receptors and moe D1 and 4
      • Most atypicals also antagonize serotonin receptor 5-HT2A (bind to them to block) to same degree as D2
      • The time the occupy D2 receptors may be different: Seeman 2002 “fast-off” theory - atypicals bind more loosely to D2 sites than conventional, so doesn't last long enough to produce side effects seen in conventional eg) tardive dyskinesia (tic-like movement of the tongue, face, mouth or whole body)
      • ‘Half-life’ of atypicals also thought to be less than conventional - atypical falls off D2 within 24 hours, conventional is longer than 24 hours


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