On the biochemical and neuropsychological mechanism of action of SSRIs in PFC of schizophrenics:

a) Any other underlying mechanisms besides GABAa receptor interaction or alteration of expression in hippocampal formation, ACC and PFC?

b) Any other biochemical mechanism or physiological pathway that can be a prospective or promising alternative explanation?

You are welcome to extend the questions, or provide more details with references about this.

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