Brain mechanisms of synchronous sleep.
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Biomedical subjects
Publications and source records attributed to M Mancia.
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Somatosensory cortical neurons were intracellularly and extracellularly recorded in cats encéphale isolé, and after acute lesions of midthalamic nuclei or after chronic hemisection of the brain stem at the pretrigeminal level. Intracellular recordings showed postsynaptic facilitatory and inhibitory effects at very low latency by stimulating both the mesencephalic (MRF) and bulbar reticular formation (BRF). Inhibitory effects dominated by stimulating the BRF. Neither midthalamic lesions nor pretrigeminal hemisection changed the quality of latency of postsynaptic responses. Extracellular recordings revealed long-latency inhibition of discharge following MRF stimulation after midthalamic lesion. In these experimental conditions long-latency BRF effects were abolished. No differences were found in responses of pyramidal tract (PT) or non-PT neurons during BRF and MRF stimulation. The results are discussed on the basis of a possible extrathalamic differential reticular control, from caudal and rostral brain stem, of somatosensory cortical neurons.
The sleep-inducing properties of a new benzodiazepine hypnotic (quazepam--SCH 16134) were evaluated in cats with transection at different levels of the brain stem structure. Effects observed after administration of doses ranging from 0.12 and 1 mg/kg given intravenously were compared with those of pentobarbital. In the encéphale isolé small doses of quazepam induced or increased the synchronized periods. The desynchronized electroencephalogram (EEG) pattern of midpontine pretrigeminal preparations was not modified by these small doses. Only larger doses induced a fast neocortical activity of high amplitude. In midpontine pretrigeminal hemisection the synchronization occurred exclusively or predominantly in the hemisphere contralateral to the lesion. In the cerveau isolé, quazepam did not influence the typical synchronized EEG pattern. The arousal threshold after mesencephalic and physiological stimulation was raised only in encéphale isolé animals. Pentobarbital provoked sustained synchronization in all preparations with a pattern quite different from that of the benzodiazepine. These results suggest that quazepam may act through facilitation of the EEG-synchronizing mechanisms localized in the lower brain stem which are involved in physiological EEG-synchronizing and sleep-inducing processes.
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Intracellular recordings were performed from bulbar and caudopontine (BcP), rostropontine (rP) and mesencephalic (Mes) neurons in acute encéphale isolé preparations during low- and high-frequency basal forebrain (BF) and hypothalamic (Hyp) stimulation. Low-frequency BF stimulation induced long-latency (7-8 msec) EPSPs on 31% of BcP neurons. High-frequency stimulation of the same regions induced excitation in 58% of them. No inhibition was observed. The descending influences on BcP neurons disappeared after bilateral acute sensorimotor decortication. Low- and high-frequency BF stimulation influenced a very low percentage of rP and Mes neurons. The only effect was a long-latency slow rising EPSP with or without spikes. No inhibition was found in these neurons. Low- and high-frequency Hyp stimulation produced short-latency EPSPs with or without spikes on a large percentage of BcP, rP and Mes neurons. The effect was more constant on rostral (rP) than on caudal (BcP) neurons and more evident when high-frequency stimulation was applied. At high frequency the activation of brain stem neurons paralleled an EEG desynchronization. IPSPs were seen in a low percentage of Mes and rP neurons. Mes neurons could be also activated antidromically. The results suggest that BF regions do not antagonize directly the mesencephalic activating system and may induce electrocortical synchronization through the activation of caudal brain stem neurons. This circuit involves sensorimotor cortical neurons. The facilitatory effect of Hyp stimulation on rostral brain stem neurons indicates that the EEG desynchronization which follows high-frequency Hyp activation may be mediated by the ascending reticular system. Other mechanisms mainly at the diencephalo-telecephalic level may however be involved in this effect.
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