Explain how atypical antipsycotic drugs may reduce cognitive impairment in schizophrenia, as well as reduce positive symptoms in schizophrenia, according to the dopamine and glutamate hypothesis of schizophrenia.
What will be an ideal response?
Ans: In schizophrenia, there are underactive mesocortical dopamine neurons that originate in the ventral tegmental area and terminate in prefrontal cortex. Diminished dopamine activity in the prefrontal cortex causes less activation of glutamate neurons that innervate the ventral tegmental area and facilitate a positive feedback loop for mesocortical dopamine neurons. Lower activity of glutamate neurons from the prefrontal cortex to the nucleus accumbens may result in less activation of GABA neurons that terminate in the ventral tegmental area. Diminished GABA neuron activity may disinhibit mesolimbic dopamine neurons, leading to increased dopamine release in the nucleus accumbens and perhaps other parts of the limbic system. Low dopamine levels in the prefrontal cortex (along with diminished glutamate activity) may account for cognitive impairment in schizophrenia. Atypical antipsychtoic drugs may correct this by elevated dopamine levels in the prefrontal cortex; in turn, elevating dopamine in the PFC will have effects throughout the system, ultimately diminishing dopamine release in the nucleus accumbens and reducing positive symptoms.
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