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Paradoxical sleep in the rat, cat and mouse is preceded and sometimes followed by a short-lasting intermediate stage characterized by high-amplitude anterior cortex spindles and low-frequency hippocampal theta rhythm. Several neurophysiological arguments suggest that the intermediate stage corresponds to a brief functional disconnection of the forebrain from the brainstem. This paper is devoted to the review of quantitative and qualitative influences of three generations of hypnotics on the intermediate stage-paradoxical sleep couple. Barbiturates, first-generation hypnotics, extend the intermediate stage at the expense of paradoxical sleep. Three benzodiazepines are compared, two with a short half-life (triazolam and midazolam) and one with a long half-life (diazepam). They also decrease sleep occurrence latency and increase the intermediate stage at the expense of paradoxical sleep, except for midazolam, which increases both the intermediate stage and paradoxical sleep at low dose. Zolpidem and zopiclone, hypnotics of third generation, decrease paradoxical sleep but the intermediate stage never substitutes for paradoxical sleep. The results are discussed in relationship to the functional aspects of this turning-point period of sleep.

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Three phospholipase A2 (PLA2s), OS1 and OS1 purified from the taipan snake venom Oxyuranus scutellatus scutellatus and bee venom PLA2 were injected to rats by the intracerebroventricular route. OS1 showed no sign of neurotoxicity at doses at which OS2 and bee venom PLA2 produced multiform dose-dependent behavioural effects including motor disturbances (stereotyped movements), compulsive scratching, convulsions and breathing difficulties. EEG recordings showed at the very time when the animal was motionless the induction of several episodes of a low frequency hippocampal theta rhythm, index of long-term changes in synaptic neuroplasticity. Spike-wave discharges were also produced but the occurrence was not systematic. These seizures were often accompanied with behavioural convulsions. Blockers of NMDA receptors and drugs modifying the GABAergic transmission could not abolish the neurotoxic effects of PLA2s except for diazepam (10 mg/kg intraperitoneally) that prevented only OS2-induced disturbances. Blockers of L-type Ca2+ channels and K+ channel openers were also without effect. The toxicity of OS2 and bee venom PLA2 is probably due to their initial specific binding to their neuronal receptor sites.

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