The negative symptoms of schizophrenia and the monoamine oxidase inhibitors

Abstract

Thirty chronic ambulatory schizophrenic patients whose main psychopathology was characterized by the persistence of negative symptoms, such as emotional withdrawal, depressed mood, motor retardation and blunted affect were included in this project in order to evaluate the therapeutic efficacy of tranylcypromine plus chlorpromazine therapy. The results show that tranylcypromine when added to the usual dose of chlorpromazine, in many instances, induces a definite improvement in these patients' clinical condition, that such treatment is safe and it may be also useful in preventing the occurrence of extra-pyramidal symptoms.

Depression in Schizophrenia: Perspective in the Era of “Atypical” Antipsychotic Agents

“…Adjunctive monoamine oxidase inhibitors (MAOIs) might also be useful for depression in schizophrenia, although the literature is sparse (142). It is of further interest that there have been some encouraging results involving adjunctive SSRIs (140,141,(143)(144)(145)(146)(147), MAOIs (141,(148)(149)(150), and trazodone (151) in double-blind trials treating negative symptoms in schizophrenia. No prospective randomized study has yet been published, however, involving an adjunctive antidepressant added to an atypical antipsychotic agent in depressed patients with schizophrenia.…”

Biochemical Findings of Negative Symptoms in Schizophrenia and Their Putative Relevance to Pharmacological Treatment

“…However, evaluating both symptom clusters, Bucci [178] observed an improvement in 17 chronically ill schizophrenic patients after chlorpromazine and tra nylcypromine.…”

Substances increasing the extracellular content of dopamine in the striatum prevent the development of haloperidol catalepsy in rats

“…An anticataleptic effect was previously described in a number of reports [1,3,4] for L-DOPA, amphetamine, MAO inhibitors, blockers of DA reuptake, and piracetam. In spite of the possible involvement of other mechanisms, the weakening of haloperidol catalepsy found by us for the action of substances under conditions of a marked increase of the extracellular DA content confirms the above hypothesis.…”

“…It is well known that the extracellular DA concentration can be increased in the striatum in the following ways: by boosting transmitter release (the potential-dependent one by blocking the terminal DA autoreceptors, of heteroreceptor influence; the potential-independent one by substances releasing DA with the aid of a carrier), by blocking the monoarnine reuptake, activating biosynthesis, and by inhibiting monoamine oxidase (MAO) activity [4,5,9,10,15]. Accordingly, the following substances were used for the study: sulpiride, an inhibitor of the terminal DA autoreceptors, which induces an additional increase of DA release in the rat striatum against the background of haloperidol [6]; piracetam, which boosts DA release in the striatum as a result of probable action on the glutamate receptors and involvement in the processes of heteroreceptor regulation [ 1]; amphetamine, which releases newly synthesized cytoplasmic DA as a result of an tetrodotoxin-insensitive process with the aid of a carrier [15], nomifenzine, an inhibitor of monoamine reuptake [5]; L-DOPA, a DA precursor [10]; and pargyline, an MAO inhibitor [9].…”