Jacobs Journal of Neurology and Neuroscience

Neuropharmacology by Benzodiazepines (Type of Medication Known As Tranquilizers)

Published on: 2019-03-30

Abstract

Although benzodiazepines (BZs) have been the most widely used sedative/hypnotics for many years, the mechanism by which they induce sleep and the neuroanatomical site(s) at which they act have remained poorly understood. Recent characterization of the central BZ-GABAA receptor complex using molecular biological techniques and sleep studies employing new ligands has begun to elucidate these issues. The pharmacologic significance of receptor subtypes also remains uncertain. A growing body of proof indicates that the hypnotic effects of BZs involve alterations in potential-dependent Ca flux. In terms of anatomy, BZ effects on sleep may result from actions in the anterior hypothalamus as well as brainstem structures including the dorsal raphe nuclei. Administration of Valium (0.5 and 2.0 mg/kg), flumazenil (5.0 and 10.0 mg/ kg) and Ro 15?4513 (1.0, 2.0 and 3.0 mg/kg) either did not affect (in low doses) or inhibited (in high doses) locomotion’s of control animals. The inhibition of motion activity by these medications was larger in sleep?deprived animals. In the plus-maze check, Valium during a dose of two.5 mg/kg had associate degree anxiolytic impact up to speed mice that was mirrored by a rise within the proportion of entries onto and therefore the share of your time spent on the open arms of the plus?maze. The convulsive actions of bicuculline (2.0–4.0 mg/kg) and picrotoxin (2.5–4.0 mg/kg) were considerably more pronounced in sleep?deprived mice as compared to control animals. The effect of pentylenetetrazol (60?100 mg/kg) was not changed in sleep-deprived mice. These data suggest that sleep deprivation induced a sensitization of mice to the motor depressant effect of benzodiazepine receptor agonists, antagonists and inverse agonists and to the convulsive action of bicuculline and picrotoxin. At the same time sleep deprivation induces a hyposensitivity of mice to the anxiolytic effect of diazepam. It is proposed that the hyposensitivity to the anxiolytic effect of diazepam as well as the hypersensitivity to the convulsions induced by bicuculline and picrotoxin in sleep-deprived mice might be due to the alterations in the function of GABA-benzodiazepine-barbiturate complex induced by sleep deprivation.

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