| pubmed-article:6668761 | pubmed:abstractText | The effects of gamma amino butyric acid (GABA), bicuculline and amino-oxyacetic acid (AOAA) on nitrazepam-induced sleep were studied in young chicks. GABA (200-3200 mg/kg) induced a marked sedation in young chicks. It also potentiated nitrazepam (1.6 mg/kg)-induced sleep. Bicuculline (1.25-5.00 mg/kg) effectively antagonized nitrazepam-induced sleep. In addition, it effectively antagonized GABA (1600 mg/kg)-induced potentiation of nitrazepam sleep. AOAA (2.5-7.5 mg/kg) delayed the onset of nitrazepam sleep, but significantly prolonged its duration. Nitrazepam (1.6 mg/kg) synchronized the electroencephalogram (EEG) of the hyperstriatum, optic tectum and reticular formation. Similarly, the electromyograph (EMG) activity was markedly reduced. GABA (1600 mg/kg) synchronized the EEG of the hyperstriatum, optic tectum and reticular formation while the EMG activity was reduced. Administration of GABA (1600 mg/kg) into nitrazepam (1.6 mg/kg)-pretreated chicks induced desynchronization of the EEG of the hyperstriatum, while the EEG of the reticular formation was synchronized. In addition, the EMG activity was reduced. Bicuculline (5 mg/kg) activated the EEG of the hyperstriatum; this effect was antagonized by GABA (1600 mg/kg). Similarly, GABA (1600 mg/kg)-induced decrease in EMG activity, synchronization of the EEG of the optic tectum and reticular formation was antagonized by bicuculline. The present data suggest that GABA potentiated nitrazepam-induced behavioral and electroencephalographical sleep. | lld:pubmed |
