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PubMed1988

[Participation of the thalamic reticular nucleus in the shaping of the interrelations of the mesencephalic reticular formation and the lateral geniculate body].

On the awake rabbits and cats under nembutal anesthesia it has been shown that the reticular nucleus of the thalamus takes considerable part in the formation of reticulogeniculate response of the lateral geniculate body (LGB) to electrostimulation of the mesencephalic reticular formation. It is assumed that the reticular nucleus of the thalamus takes basic part in a realization of "rapid" physical influences of the reticular formation on the LGB.

Animals↗
PubMed1986

Brain temperature in the rat midbrain reticular formation is regulated by bombesin and TRH.

We investigated the effects of intraventricular (ivt) injection of bombesin on the TRH-induced increase in temperature in the midbrain reticular formation (mrf) of the rat brain under pentobarbital anesthesia. Ivt injection of TRH in a dose of 3 nmol significantly antagonized the decrease in brain temperature induced by pentobarbital, and this antagonistic action of TRH was dose-related. Ivt injection of 3-300 pmol bombesin produced a dose-related decrease in brain temperature in response to 3 nmol TRH injection. The present data provide evidence that bombesin and TRH produce opposite actions on thermoregulation of the mrf in the rat.

Animals↗
PubMed1989

Role of pontomedullary reticular formation neurons in horizontal head movements: an ibotenic acid lesion study in the cat.

Single-cell recording, electrolytic lesion and electrical stimulation studies have indicated that the pontomedullary reticular formation (PMRF) plays a role in head movement (HM) control. However, recent studies utilizing excitotoxin lesions of the PMRF have reported no effect on HM. In the present study, we have examined the acute and chronic motor effects of injecting ibotenic acid (IBO) into the nucleus reticularis pontis oralis, nucleus reticularis pontis caudalis and rostral medullary nucleus gigantocellularis of the feline PMRF. IBO injections in all of these regions induced tonic flexion of the head toward the ipsilateral side. This effect lasted 4-16 h. It was followed by a second phase in which head flexion and whole body circling were directed toward the contralateral side. Although this forced contralateral head turning disappeared within two days, the tendency to turn contralaterally and the impaired ability to make rapid ipsilateral HMs were present throughout survival periods lasting more than 4 months. Unilateral IBO PMRF lesions reduced the amplitude of vestibular induced quick phase (anti-compensatory) HMs toward the ipsilateral side and resulted in abnormally large and persistent slow compensatory HMs toward the contralateral side. Following IBO injections, the threshold intensity for HMs evoked by electrical stimulation at the injection site was elevated, and the amplitude and velocity of evoked HMs reduced. Histological data indicated that the reticular area involved in HM control was relatively large and probably extended beyond the PMRF region examined here. However, lesions including the nucleus reticularis pontis caudalis (NRPC) produced more severe and persistent HM deficits than those including the nucleus reticularis gigantocellularis. These data together with available anatomical and electrophysiological evidence indicate that PMRF neurons play a critical role in the generation of fast horizontal HMs toward the ipsilateral side.

Action Potentials↗
PubMed1991

Incisor growth acceleration after lesions in the lateral pontine reticular formation of rats.

The length of upper and lower incisors of Long-Evans hooded rats between gingiva and top were measured before and after small bilateral symmetric electrolytic lesions of the pontine reticular formation between the ventromedial parabrachial nucleus and the motor trigeminal nucleus. Ten days after lesions of this region 8.5 mm posterior to bregma the length of upper incisors was 13.4 +/- 0.7 mm compared with 6.1 +/- 0.2 mm before lesion (p less than 0.01) and the length of the lower incisors 17.1 +/- 0.4 mm compared with 10.2 +/- 0.2 mm before lesion (p less than 0.01). A second group with a smaller lesion of this region 9.0 mm posterior to bregma reached upper incisor length of 13.2 +/- 0.4 mm (p less than 0.05) and lower incisor length of 14.7 +/- 0.5 mm (p less than 0.05) at the 20th postoperative day. Sham-operated controls had no tooth growth acceleration.

Animals↗
PubMed1989

Monosynaptic nigral inputs to the pedunculopontine tegmental nucleus neurons which send their axons to the medial reticular formation in the medulla oblongata. An electron microscopic study in the cat.

An electron microscopic study in the cat has suggested that neurons in the substantia nigra pars reticulata (SNr) project to the medial reticular formation of the medulla oblongata (MRF) via the pedunculopontine tegmental nucleus (PPN): PPN neurons, which were labeled with a retrograde tracer (WGA-HRP; horseradish peroxidase conjugated to wheat germ agglutinin) injected into the MRF, were found to be in synaptic contact with axon terminals which were degenerated with neurotoxic agents applied into the SNr.

Animals↗
PubMed1999

REM sleep enhancement and behavioral cataplexy following orexin (hypocretin)-II receptor antisense perfusion in the pontine reticular formation.

Orexin (hypocretin)-containing neurons of the hypothalamus project to brainstem sites that are involved in the neural control of REM sleep, including the locus coeruleus, the dorsal raphe nucleus, the cholinergic zone of the mesopontine tegmentum, and the pontine reticular formation (PRF). Orexin knockout mice exhibit narcolepsy/cataplexy, and a mutant and defective gene for the orexin type II receptor is present in dogs with an inherited form of narcolepsy/cataplexy. However, the physiological systems mediating these effects have not been described. We reasoned that, since the effector neurons for the majority of REM sleep signs, including muscle atonia, were located in the PRF, this region was likely implicated in the production of these orexin-related abnormalities. To test this possibility, we used microdialysis perfusion of orexin type II receptor antisense in the PRF of rats. Ten to 24 hours after antisense perfusion, REM sleep increased two- to three-fold during both the light period (quiescent phase) and the dark period (active phase), and infrared video showed episodes of behavioral cataplexy. Moreover, preliminary data indicated no REM-related effects following perfusion with nonsense DNA, or when perfusion sites were outside the PRF. More work is needed to provide precise localization of the most effective site of orexin-induced inhibition of REM sleep phenomena.

Animals↗