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At least 631 records · Page 35Linked to original sources
PubMed1989

REM sleep enhancement induced by sensory stimulation is prevented by kainic acid lesion of the pontine reticular formation.

It has been shown that auditory or somatic stimulation during rapid eye movement (REM) sleep is capable of producing a significant increase in ponto-geniculo-occipital (PGO) spike density as well as in REM sleep duration. The purpose of this study was to determine the role of the medial pontine reticular formation (PRF) in mediating such increase of REM sleep duration. After a baseline recording whereby on the same recording day the control and the stimulus (auditory or somatic) alternated with each REM, a group of cats was lesioned with kainic acid in the PRF. The sleep-wake cycle was recorded again on days 15, 30 and 45 post-lesion, following the same procedure. The results showed no changes in REM sleep duration and PGO spike density in the lesioned animals. However, when sensory stimulation was applied it was ineffective in producing REM sleep enhancement, although it was able to increase PGO spike density. These findings suggest that the effects of sensory stimulation on REM sleep duration are accomplished through the PRF, probably by inducing an increase in the excitability levels of such neurons, and further suggests that PGO spike density and REM duration are independent of each other.

Acoustic Stimulation↗
PubMed2005

Hypocretin (orexin) receptor subtypes differentially enhance acetylcholine release and activate g protein subtypes in rat pontine reticular formation.

The hypothalamic peptides hypocretin-1 (orexin A) and -2 (orexin B) promote wakefulness by mechanisms that are not well understood. Defects in hypocretinergic neurotransmission underlie the human sleep disorder narcolepsy. Hypocretins alter cell excitability via two receptor subtypes, hypocretin receptor subtype 1 (hcrt-r1) and hypocretin receptor subtype 2 (hcrt-r2). This study aimed to identify G protein subtypes activated by hypocretin in rat pontine reticular nucleus oral part (PnO) and the hypocretin receptor subtype modulating acetylcholine (ACh) release in the PnO. G protein activation was quantified using in vitro [(35)S]guanylyl-5'-O-(gamma-thio)triphosphate autoradiography. ACh release was measured using in vivo microdialysis and high-performance liquid chromatography. Hypocretin-1-stimulated G protein activation was significantly decreased by pertussis toxin, demonstrating that some hypocretin receptors in rat PnO activate inhibitory G proteins. Hypocretin-1-stimulated ACh release was not blocked by pertussis toxin, supporting the conclusion that the hypocretin receptors modulating ACh release in rat PnO activate stimulatory G proteins. Hypocretin-1 and -2 each caused a concentration-dependent increase in ACh release with similar potencies, indicating that hcrt-r2 modulates ACh release in PnO. Hypocretin-1 caused a significantly greater increase in ACh release than hypocretin-2, suggesting a role for hcrt-r1 in the modulation of PnO ACh release. Taken together, these data provide the first evidence that hypocretin receptors in rat PnO signal via inhibitory and stimulatory G proteins and that ACh release in rat PnO is modulated by hcrt-r2 and hcrt-r1. One mechanism by which hypocretin promotes arousal may be to increase ACh release in the pontine reticular formation.

Acetylcholine↗
PubMed1985

[Features of the activation of neurons of the reticular formation of the brain stem in the cat to somatic stimuli of various modality].

Neuronal responses of two reticular structures--nucleus reticularis pontis caudalis (RPC) and nucleus reticularis gigantocellularis (RGC)--to electrical nociceptive stimulation of the internal intercostal nerve and non-nociceptive, tactile stimulation of the skin in the same somatic area have been studied in chloralose anesthetized cats. It was shown that the mean number of action potentials in responses of RPC-neurons to tactile stimulation exceeded that for FGC-neurons by 20-150%. On the opposite, the average number of action potentials in RPC-neurons in response to nerve stimulation was lower by 15-54% than those of bulbar neurons. Data obtained indicate the existence of spatial rostro-caudal differentiation of somatosensory modalities in the reticular brainstem formation.

Animals↗
PubMedDate not supplied

The role of the sympathetic system in producing cardiac disturbances determined by stimulation of the midbrain reticular formation in the cat.

The authors check the theory according to which cardiac rhythm disturbances developing after myocardial infarction or in the course of a long Q-T interval syndrome are due to stimulation of the autonomic nervous system which innervates the heart via the stellate ganglia, the tonus of the left sympathetic being predominant over the right sympathetic at cardiac level. Six semiacute experiments were carried out on curarized cats in which arrhythmia was produced by stereotaxic electric stimulation of the midbrain reticular formation (MRF). Stimulation of MRF after either left or right stellectomy induced the same type of rhythm disturbances as that produced before stellectomy (ventricular extrasystoles and idioventricular paroxysmal tachycardia); however, latency in the development of these rhythm disturbances significantly increased after left stellectomy. After bilateral removal of the stellate ganglia, stimulation of the MRF only induced isolated or clustered ventricular extrasystoles. The results suggest that both stellate ganglia have an almost equal determinant role in the appearance of cardiac system disturbances obtained by stimulation of the MRF, the left having a somewhat more rapid effect.

Animals↗