Schizophrenia reserpine treatment

Reserpine inhibits the synaptic vesicular storage of the monoamines dopamine, serotonin and noradrenaline. As a result they leak out into the cytoplasm where they are inactivated by monoamine oxidase this causes their long-lasting depletion. The resulting low levels of dopamine underlie the antipsychotic actions of reserpine (Chapter 11), whereas the reduced noradrenaline levels underlie its antihypertensive actions. Finally, the resulting low levels of serotonin and noradrenaline mean that reserpine also induces depression. These severe side effects mean that reserpine is no longer used clinically as a treatment for schizophrenia (Chapter 11). 

Reserpine A drug extracted from Rauwolfia serpentina which was once clinically used in the treatment of essential hypertension and schizophrenia. 

It potentiates (already in low doses) the excitement syndrome induced by DOPA and simultaneously annihilates the depression caused by reserpine. In man, 74 seems to be useful in the treatment of psychoses and schizophrenia. 

A prolonged period of increased motor activity after starting reserpine ( reserpine-reversal ) possibly occurred in 3 patients with schizophrenia treated firstly with phenelzine for 12 weeks, then a placebo for 16 to 33 weeks, and lastly reserpine for 12 weeks, when compared with patients receiving reserpine who had not received an MAOI. Their blood pressures rose slightly and persistently, and their psychomotor activity was considerably increased, lasting in two cases throughout the 12-week period of treatment. ... 

Tetrabenazine was synthesized in the 1950s as part of research into compounds with reserpine-Uke activity and was initially used in the treatment of schizophrenia. Its common reversible adverse effects include drowsiness/sedation, weakness, parkinsonism, depression, and acute akathisia. 

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