Localization of efferent function in the dorsal motor nucleus of the vagus

Laughton, Watson B.; Powley, Terry L.

doi:10.1152/ajpregu.1987.252.1.r13

Cited by 42 publications

(36 citation statements)

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“…24 If we can assume a similar spread of ethanol from the RVL to the nucleus ambiguus as occurred from the NTS to the DMV, there should have been a greater impairment of baroreceptor reflex control of heart rate when ethanol was injected into the RVL because of the greater role of the nucleus ambiguus than the DMV in controlling central vagal tone in the rat. 25 However, the magnitude of the impairment of the baroreceptor heart rate response was much less after injection of ethanol into the RVL than the NTS. Thus, it is unlikely that the nucleus ambiguus was involved, as a primary site, in the inhibitory action of ethanol after its microinjection into the RVL.…”

Section: Discussionmentioning

confidence: 96%

Impairment of baroreceptor reflex control of heart rate but not sympathetic efferent discharge by central neuroadministration of ethanol.

1989

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We investigated the acute hemodynamic effects of ethanol microinjection into brain areas known to influence cardiovascular function and reflexes. In chloralose-anesthetized rats, ethanol had no effect on baseline mean arterial pressure, heart rate, or sympathetic efferent discharge when microinjected into the nucleus tractus solitarius, the dorsal motor nucleus of the vagus, the rostral ventrolateral medulla, or the posterior hypothalamus. On the other hand, ethanol microinjection into the anterior hypothalamus caused a site-dependent pressor effect and an increase in sympathetic efferent discharge. Baroreceptor heart rate response but not sympathetic efferent discharge response was impaired by ethanol microinjection into the nucleus tractus solitarius, the dorsal motor nucleus of the vagus, and the rostral ventrolateral medulla, suggesting that ethanol involves one or more of these areas in its inhibitory effect on baroreceptor heart rate response and that ethanol has a selective action on baroreceptor reflex control of heart rate. The findings that 1) the effect was dose dependent and 2) injection of ethanol outside of, or an equal volume of cerebrospinal fluid into, the nucleus tractus solitarius had no effect on the response strongly suggest that the observed effect on baroreceptor heart rate response was ethanol mediated. Ethanol microinjection into the dorsal motor nucleus of the vagus impaired the heart rate response, thus raising the possibility that leakage of ethanol to that area from the nucleus tractus solitarius might have contributed to its effect. These findings show that ethanol has a pressor and sympathoexcitatory site of action within the anterior hypothalamus and that it selectively impairs baroreceptor heart rate response via a central site of action; the mechanisms by which ethanol produces these effects remain to be elucidated.

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Section: Discussionmentioning

confidence: 96%

Impairment of baroreceptor reflex control of heart rate but not sympathetic efferent discharge by central neuroadministration of ethanol.

1989

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“…Since the dorsal vagal neurons innervate several organs of the gastrointestinal tract, their metabolism-gated K + channels may be involved in nutritive functions. Accordingly, stimulation of the dorsal vagal nucleus in vivo results in a substantial release of insulin as a subpopulation of dorsal vagal neurons innervates pancreatic β-cells (Laughton and Powley, 1987). In line with a putative role in glucose homeostasis, the KATP channels of the dorsal vagal neurons are not only activated by anoxia but also by a fall of interstitial glucose levels (Ballanyi et al, 1996a).…”

Section: Katp Channels In Anoxia-tolerant Dorsal Vagal Neuronsmentioning

confidence: 96%

Protective role of neuronal KATP channels in brain hypoxia

Ballanyi

2004

Journal of Experimental Biology

129

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SUMMARY During severe arterial hypoxia leading to brain anoxia, most mammalian neurons undergo a massive depolarisation terminating in cell death. However,some neurons of the adult brain and most immature nervous structures tolerate extended periods of hypoxia–anoxia. An understanding of the mechanisms underlying this tolerance to oxygen depletion is pivotal for developing strategies to protect the brain from consequences of hypoxic-ischemic insults. ATP-sensitive K+ (KATP) channels are good subjects for this study as they are activated by processes associated with energy deprivation and can counteract the terminal anoxic-ischemic neuronal depolarisation. This review summarises in vitro analyses on the role of KATP channels in hypoxia–anoxia in three distinct neuronal systems of rodents. In dorsal vagal neurons, blockade of KATPchannels with sulfonylureas abolishes the hypoxic-anoxic hyperpolarisation. However, this does not affect the extreme tolerance of these neurons to oxygen depletion as evidenced by a moderate and sustained increase of intracellular Ca2+ (Cai). By contrast, a sulfonylurea-induced block of KATP channels shortens the delay of occurrence of a major Cai rise in cerebellar Purkinje neurons. In neurons of the neonatal medullary respiratory network, KATP channel blockers reverse the anoxic hyperpolarisation associated with slowing of respiratory frequency. This may constitute an adaptive mechanism for energy preservation. These studies demonstrate that KATP channels are an ubiquituous feature of mammalian neurons and may, indeed, play a protective role in brain hypoxia.

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“…The DMN provides the major source of innervation to the stomach (24) and, in addition, it has been demonstrated that neurons within this nucleus play an important role in the control of gastric acid secretion (13,25,26). The DMN has been shown to contain a number of neurons and processes that exhibit inmunoreactivity to nNOS (16).…”

Section: Fig 7 Distribution Of Nnos Immunoreactive Neural Structuresmentioning

confidence: 99%

Inhibition of gastric acid secretion by stress: A protective reflex mediated by cerebral nitric oxide

Esplugues

Barrachina

Beltrán

et al. 1996

Proc. Natl. Acad. Sci. U.S.A.

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Moderate somatic stress inhibits gastric acid secretion. We have investigated the role of endogenously released NO in this phenomenon. Elevation of body temperature by 3؇C or a reduction of 35 mmHg (1 mmHg ‫؍‬ 133 Pa) in blood pressure for 10 min produced a rapid and long-lasting reduction of distension-stimulated acid secretion in the rat perfused stomach in vivo. A similar inhibitory effect on acid secretion was produced by the intracisternal (i.c.) administration of oxytocin, a peptide known to be released during stress. Intracisternal administration of the NO-synthase inhibitor, N G -nitro-L-arginine methyl ester (L-NAME) reversed the antisecretory effect induced by all these stimuli, an action prevented by intracisternal coadministration of the NO precursor, L-arginine. Furthermore, microinjection of L-NAME into the dorsal motor nucleus of the vagus nerve reversed the acid inhibitory effects of mild hyperthermia, i.v. endotoxin, or i.c. oxytocin, an action prevented by prior microinjection of L-arginine. By contrast, microinjection of L-NA ME into the nucleus tractus solitarius failed to affect the inhibitory effects of hyperthermia, i.v. endotoxin, or i.c. oxytocin. Immunohistochemical techniques demonstrated that following hyperthermia there was a significant increase in immunoreactivity to neuronal NO synthase in different areas of the brain, including the dorsal motor nucleus of the vagus. Thus, our results suggest that the inhibition of gastric acid secretion, a defense mechanism during stress, is mediated by a nervous ref lex involving a neuronal pathway that includes NO synthesis in the brain, specifically in the dorsal motor nucleus of the vagus.

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Localization of efferent function in the dorsal motor nucleus of the vagus

Cited by 42 publications

References 0 publications

Impairment of baroreceptor reflex control of heart rate but not sympathetic efferent discharge by central neuroadministration of ethanol.

Impairment of baroreceptor reflex control of heart rate but not sympathetic efferent discharge by central neuroadministration of ethanol.

Protective role of neuronal KATP channels in brain hypoxia

Inhibition of gastric acid secretion by stress: A protective reflex mediated by cerebral nitric oxide

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