Nitric oxide synthase (NOS) is an enzyme involved in the activation of the glutamate/NMDA receptor-induced cascade of events. In this study we investigated the NOS activity in different rat brain regions after chronic electroconvulsive, imipramine and citalopram treatments. Chronic electroconvulsive treatment significantly increased the NOS activity (by 49%) in the cerebral cortex. However, chronic treatment with imipramine or citalopram did not alter the activity of NOS in all examined brain regions (cortex, hippocampus or cerebellum). The increased NOS activity after electroconvulsive but not pharmacologic (imipramine or citalopram) treatment may well reflect the differences between the adaptive changes of the NMDA receptor complex induced by these treatments.

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PubMedDate not supplied

Preparation and investigation of inclusion complexes containing nitrazepam.

Nitrazepam is a valuable drug, being one of the often used minor tranquillizers in psychotherapy. However, its solubility characteristics are very unfavourable. Products were prepared with dimethyl-beta-cyclodextrin in different combinations (8.58%, 19.48% and 27.29%) and by several methods such as mixing, kneading, precipitation and spray-drying.

Cyclodextrins↗

PubMedDate not supplied

Chronic electroconvulsive treatment increases the activity of nitric oxide synthase in the rat brain.

Activation of the NMDA receptor complex increases the intracellular free Ca2+ concentration, which in turn influences a nitric oxide synthase (NOS) activity. In this study we investigated the NOS activity after acute and chronic electroconvulsive treatment in different rat brain regions. Chronic (10 daily treatments) but not acute (single treatment) significantly increased the NOS activity by 60% in the cerebral cortex and by 20-30% in hippocampus and cerebellum. The increased NOS activity might be a compensatory mechanism which balanced the reduced NMDA receptor complex reactivity. In fact, the adaptation of the NMDA receptor complex induced by chronic electroconvulsive treatment (and antidepressant drugs) measured at the receptor level, suggests the subsensitivity of that complex. Present results support the hypothesis of the critical role of the NMDA receptor pathway in the mechanism of antidepressant action.

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PubMedDate not supplied

Effect of kainic acid and pentetrazole administration on the activity of nitric oxide synthase in the mouse brain.

The present study examined ex vivo effect of kainic acid and pentetrazole administration on the activity of nitric oxide synthase (NOS) in the mouse brain. NOS activity was assayed by measuring the formation of [3H] citrulline from [3H]arginine in the homogenates of mouse hippocampus, neocortex and cerebellum. The highest basal activity of the enzyme was found in this latter brain region. Administration of kainic acid (30 mg/kg) increased the NOS activity in all brain regions examined. On the other hand, pentetrazole (60 mg/kg) did not evoke any significant changes in the NOS activity at 5 min after the administration. Only in cerebellum, at 10 min after administration of pentetrazole, the increase in the activity of the enzyme was observed. The obtained results indicate that the two particular convulsants used in this study differ not only in respect of behavioral signs of seizures which they evoke, but also in respect of the effect on mouse brain NOS activity.

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