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Sleep is differently modulated by basal forebrain [GABA.sub.A] and [GABA.sub.B] receptors. Am J Physiol Regulatory Integrative Comp Physiol 281: R170-R175, 2001.--There is evidence that GABA plays a major role in sleep regulation. [GABA.sub.A] receptor agonists and different compounds interacting with the [GABA.sub.A] receptor complex, such as barbiturates and benzodiazepines, can interfere with the sleep/wake cycle. On the other hand, there is very little information about the possible role of [GABA.sub.B] receptors in sleep modulation. The nucleus basalis of Meynert (NBM), a cholinergic area in the basal forebrain, plays a pivotal role in the modulation of sleep and wakefulness, and both [GABA.sub.A] and [GABA.sub.B] receptors have been described within the NBM. This study used unilateral infusions in the NBM to determine the effects of 3-hydroxy-5-aminomethylisoxazole hydrobromide (muscimol hydrobromide, a [GABA.sub.A] receptor subtype agonist) and [Beta]-(aminomethyl)-4-chlorobenzenepropanoic acid (baclofen, a [GABA.sub.B] receptor subtype agonist) on sleep parameters in freely moving rats by means of polygraphic recordings. Muscimol (0.5 nmol) and baclofen (0.7 nmol) induced an increase in slow-wave sleep and an inhibition of wakefulness. Muscimol, but not baclofen, also caused a decrease in desynchronized sleep parameters. The results reported here indicate that 1) the NBM activation of both [GABA.sub.A] and [GABA.sub.B] receptors influences the sleep/wake cycle, and 2) [GABA.sub.A] but not [GABA.sub.B] receptors are important for desynchronized sleep modulation, suggesting that the two GABAergic receptors play different roles in sleep modulation. desynchronized sleep; nucleus basalis of Meynert; muscimol; baclofen

Assesses how gamma-aminobutyric acid manipulations of the rat nucleus basalis of Meynert (NBM) affected sleep and wakefulness parameters. Increase in the amount of time spent in slow-wave sleep (SWS) and SWS latency; Evidence that NBM cholinergic neurons promote cortical arousal; Effect of muscimol on desynchronized sleep.

The ability of neuroglia to buffer local increases of extracellular K(+) has been known from in vitro studies. This property may confer on these cells an active role in the modulation and spreading of cortical oscillatory activities. We addressed the question of the spatial buffering in vivo by performing single and double intraglial recordings, together with measures of the extracellular K(+) and Ca(2+) concentrations ([K(+)](out) and [Ca(2+)](out)) in the cerebral cortex of cats under ketamine and xylazine anesthesia during patterns of slow sleep oscillations and spike-wave seizures. In addition, we estimated the fluctuations of intraglial K(+) concentrations ([K(+)](in)). Measurements obtained during the slow oscillation indicated that glial cells phasically take up part of the extracellular K(+) extruded by neurons during the depolarizing phase of the slow oscillation. During this condition, the redistribution of K(+) appeared to be local. Large steady increases of [K(+)](out) and phasic potassium accumulations were measured during spike-wave seizures. In this condition, [K(+)](in) rose before [K(+)](out) if the glial cells were located at some distance from the epileptic focus, suggesting faster K(+) diffusion through the interglial syncytium. The simultaneously recorded [Ca(2+)](out) dropped steadily during the seizures to levels incompatible with efficient synaptic transmission, but also displayed periodic oscillations, in phase with the intraseizure spike-wave complexes. In view of this fact, and considering the capability of K(+) to modulate neuronal excitability both at the presynaptic and postsynaptic levels, we suggest that the K(+) long-range spatial buffering operated by glia is a parallel synchronizing and/or spreading mechanism during paroxysmal oscillations.