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At least 757 records · Page 42Linked to original sources
PubMed2002

Nociceptin inhibits gamma-aminobutyric acidergic inputs to cardiac parasympathetic neurons in the nucleus ambiguus.

Studies have shown that nociceptin, the endogenous ligand for the opioid receptor-like receptor (ORL(1)), modulates central control of cardiovascular activity. The nucleus ambiguus, an area containing cardiac parasympathetic neurons, contains both ORL(1) receptors and neurons that contain nociceptin itself. Although previous work has shown that nociceptin acts to increase parasympathetic outflow to the heart, the mechanisms by which this is achieved are unknown. In the present study, the effects of nociceptin on spontaneous gamma-aminobutyric acidergic (GABAergic) input to cardiac parasympathetic neurons (IPSCs) was examined. At 100 microM, nociceptin inhibited both the frequency (-35.6%) and the amplitude (-49.5%) of spontaneous GABAergic IPSCs in cardiac vagal neurons. Nociceptin also caused a novel postsynaptic inhibition of the responses evoked by exogenous application of GABA. These results indicate that nociceptin acts both on neurons precedent to cardiovascular neurons to decrease the activity of GABAergic neurons that synapse upon cardiovascular neurons and directly, inhibiting the postsynaptic currents evoked by GABA. This inhibition by nociceptin would increase parasympathetic outflow to the heart, thus providing a possible mechanism for nociceptin-induced bradycardia.

Animals↗
PubMed1997

Limited excitatory local effector function of gastric vagal afferent intraganglionic terminals in rats.

Intraganglionic laminar endings (IGLEs) are complex terminal structures of vagal afferent origin, distributed throughout the myenteric plexus of the esophagus and gastrointestinal tract and without a known function. They may serve local effector function by means of peripheral axon reflexes, analogously to dorsal root afferents. To test this possibility, vagal afferent fibers were antidromically activated by suprathreshold electrical stimulation of the cervical vagus nerve in anesthetized rats that underwent prior supranodose vagotomy, and responses of myenteric neurons were monitored with Fos immunocytochemistry. Stimulation of vagal afferents produced Fos expression in a slightly, but significantly, higher proportion of myenteric plexus neurons of the gastric corpus (1.02 +/- 0.21%, P < 0.05) and esophagus (1.59 +/- 0.46%, P < 0.05) than in control animals with sham-stimulation (corpus, 0.12 +/- 0.05%; esophagus, 0.18 +/- 0.18%). Stimulation of vagal efferents produced widespread Fos induction in myenteric neurons. Given the many enteric neurons in close anatomic contact with IGLEs and the low proportion of Fos activated neurons after selective afferent stimulation, the results do not support a widespread excitatory local effector function of IGLEs. However, inhibitory effects and/or weak excitatory synaptic inputs that do not engage Fos expression cannot be ruled out.

Analysis of Variance↗
PubMed1997

Phase dependencies of the human baroreceptor reflex.

We studied the influence of respiratory and cardiac phase on responses of the cardiac pacemaker to brief (0.35-s) increases of carotid baroreceptor afferent traffic provoked by neck suction in seven healthy young adult subjects. Cardiac responses to neck suction were measured indirectly from electrocardiographic changes of heart period. Our results show that it is possible to separate the influences of respiratory and cardiac phases at the onset of a neck suction impulse by a product of two factors: one depending only on the respiratory phase and one depending only on the cardiac phase. This result is consistent with the hypothesis that efferent vagal activity is a function of afferent baroreceptor activity, whereas respiratory neurons modulate that medullary throughput independent of the cardiac phase. Furthermore, we have shown that stimulus broadening and stimulus cropping influence the outcome of neck suction experiments in a way that makes it virtually impossible to obtain information on the phase dependency of the cardiac pacemaker's sensitivity to vagal stimulation without accurate knowledge of the functional shape of stimulus broadening.

Adult↗
PubMed2006

Ventilatory response to hyperoxia in newborn mice heterozygous for the transcription factor Phox2b.

Heterozygous mutations of the transcription factor PHOX2B have been found in most patients with central congenital hypoventilation syndrome, a rare disease characterized by sleep-related hypoventilation and impaired chemosensitivity to sustained hypercapnia and sustained hypoxia. PHOX2B is a master regulator of autonomic reflex pathways, including peripheral chemosensitive pathways. In the present study, we used hyperoxic tests to assess the strength of the peripheral chemoreceptor tonic drive in Phox2b+/-newborn mice. We exposed 69 wild-type and 67 mutant mice to two hyperoxic tests (12-min air followed by 3-min 100% O2) 2 days after birth. Breathing variables were measured noninvasively using whole body flow plethysmography. The initial minute ventilation decrease was larger in mutant pups than in wild-type pups: -37% (SD 13) and -25% (SD 18), respectively, P<0.0001. Furthermore, minute ventilation remained depressed throughout O2 exposure in mutants, possibly because of their previously reported impaired CO2 chemosensitivity, whereas it returned rapidly to the normoxic level in wild-type pups. Hyperoxia considerably increased total apnea duration in mutant compared with wild-type pups (P=0.0001). A complementary experiment established that body temperature was not influenced by hyperoxia in either genotype group and, therefore, did not account for genotype-related differences in the hyperoxic ventilatory response. Thus partial loss of Phox2b function by heterozygosity did not diminish the tonic drive from peripheral chemoreceptors.

Animals↗
PubMed1996

Reorganization of the innervation of the vas deferens after sympathetic decentralization.

Reorganization of autonomic efferent pathways to the rat vas deferens was noted after chronic (30 days) sympathetic decentralization produced by hypogastric nerve (HGN) transection. In normal rats, electrical stimulation of the HGN elicited an increase in vasal pressure (VP) bilaterally, whereas pelvic nerve (PN) stimulation did not alter VP. However, after unilateral HGN transection, stimulation of the PN on the transected side but not on the normal side increased VP. The decentralized vas exhibited larger VP responses to stimulation of the contralateral HGN in comparison with the normal vas. After bilateral HGN transection, PN-induced VP responses were elicited at lower stimulus intensities than in rats with unilateral transections. PN-induced VP responses were blocked by hexamethonium and prazosin but were not altered by atropine. Distension of the vas lumen occurred after decentralization. PN-induced VP responses were not detectable in extremely distended vas. These data indicate that, after degeneration of sympathetic preganglionic axons, decentralized adrenergic ganglion cells are reinnervated by parasympathetic or sympathetic preganglionic pathways and that the reinnervation influences vasal function.

Animals↗