Ventral Tegmental Nucleus Of Gudden Research Articles

Behavioral evidence for a cholinoceptive pontine inhibitory area: Descending control of spinal motor output and sensory input

Earlier studies have shown that microinjection of the cholinergic agonist carbamylcholine (carbachol) into the rostral pontine tegmentum of the cat elicits postural atonia. However, conflicting reports exist regarding other concomitant behavioral changes. The present study has demonstrated that a variety of functions supporting animals' responsiveness to external stimuli including postural somatomotor, sympathetic visceromotor and nociceptive somatosensory functions are differentially affected depending upon the injection sites. Sites associated with maximal effects on each of these functions are clustered in the dorsal pontine tegmentum, i.e. cholinoceptive pontine inhibitory area (CPIA). In a medial area of CPIA, which corresponds to an area caudal to the ventral tegmental nucleus of Gudden and ventromedial to the principal nucleus of locus coeruleus, postural somatomotor and sympathetic visceromotor functions were maximally suppressed. In a laterally adjacent area ventral to the principal nucleus of locus coeruleus, somatomotor function was predominantly suppressed. Nociceptive somatosensory function was primarily suppressed following microinjections into a more lateral area surrounding the lateral half of the brachium conjunctivum. Several lines of evidence suggest that each of these phenomena ultimately involves descending influences on the spinal motor output and/or sensory input. There was no correlation between maximal suppression of these spinal cord functions and signs of desynchronized sleep such as rapid eye movement. Carbachol microinjection into wide areas of CPIA also suppressed orienting behaviors. Taken together, these data suggest that CPIA is a system which primarily regulates animals' responsiveness to external stimuli, in part by influencing segmentally organized behaviors.

Ontogeny of cholecystokinin-8 containing neuron system of the rat: An immunohistochemical analysis—II. Lower brain stem

The ontogeny of the cholecystokinin-8 neuron system in the lower brain stem of the rat was investigated by means of indirect immunofluorescence. Cholecystokinin-8-like immunoreactive structures first appeared in the primordium of the ventral tegmental area, ventral tegmental nucleus of Gudden and the area lateral to the superior central nucleus of the fetus on gestational day 17. Although cholecystokinin-8-like immunoreactive structures appeared gradually in various lower brain stem areas from this day, and developed markedly from postnatal day 6, thereafter, the ontogeny of cells and fibers was different. In general, the fibers increased in number as the rats grew and reached the maximum in adulthood, whereas the cells reached a maximum number between postnatal days 6–12, after which they decreased in number. Colchicine treatment, however, demonstrated the presence of cholecystokinin-8-like immunoreactive cells in various areas of the lower brain stem. These findings suggest that the cholecystokinin-containing neuron system is active in the adult and that cholecystokinin-containing cell somata cannot store a sufficient amount of the peptide for visualization in the absence of colchicine. Thus, it might be concluded that cholecystokinin may play an important role in the brain function of the adult as a neurotransmitter or neuromodulator, though its exact function is now open to discussion.

Intra-raphe muscimol induced hyperactivity depends on ascending serotonin projections

Acute microinjections of the GABA agonist, muscimol (100 ng), into either the dorsal (DR) or the median (MR) raphe nucleus of etherized rats induced post-anesthesia hyperactivity as measured in photocell chambers. The increased activity counts seen after MR injections, furthermore, were 4 times greater than those following DR injections. In animals implanted with chronically indwelling cannulae, a muscimol (25–400 ng) dose-response analysis confirmed the greater sensitivity of the MR site. Subsequent experiments thus employed only MR cannulae. The benzodiazepine, chlordiazepoxide, in a subataxic dose (3.8 mg/kg, IP) by itself did not affect activity level, but enhanced the locomotor response to low doses (25–50 ng) of muscimol. Conversely, a sub-convulsant dose of the GABA antagonist, bicuculline (1.1 mg/kg, IP), completely blocked the hyperactivity produced by muscimol (50–100 ng). Bilateral electrolytic destruction of the ventral tegmental nuclei of Gudden produced hyperactivity, but failed to alter the effect of muscimol. Forebrain 5-hydroxytryptamine (5-HT, serotonin) depletion following administration of 5,7-dihydroxytryptamine did not affect baseline activity level, but markedly attenuated the locomotor response produced by intra-MR injections of muscimol. These data suggest that midbrain GABA neurons modulate activity level through a direct action on 5-HT neurons, and indicate that intra-MR muscimol induced hyperactivity depends on intact ascending 5-HT fibers.

Lesions in Gudden's tegmental nuclei produce behavioral and 5-HT effects similar to those after raphe lesions

Lesions largely restricted to the dorsal and ventral tegmental nuclei of Gudden (GTN) produced several effects similar to those seen after midbrain raphe lesions. GTN lesions significantly reduced the 5-hydroxytryptamine (5-HT) concentration of the diencephalon (31 percent), hippocampus (59 percent), and remaining portion of the telencephalon (29 percent). Striatal 5-HT, however, was not affected. GTN lesions enhanced activity in an enclosed field and facilitated two-way avoidance acquisition. Pain sensitivity as measured by the flinch-jump method was not affected. These results suggest that the GTN may be the origin of ascending 5-HT fibers and may be involved in the regulation of activity level and the adaptation of an animal to aversive situations. Thus, some of the behavioral and 5-HT effects of lesions in the midbrain raphe nuclei may be due to their involvement of the GTN and associated pathways.