Glutamate activation of neurons in CV-reactive areas of cat brain stem affects urinary bladder motility

1993 ◽  
Vol 265 (4) ◽  
pp. F520-F529 ◽  
Author(s):  
S. Y. Chen ◽  
S. D. Wang ◽  
C. L. Cheng ◽  
J. S. Kuo ◽  
W. C. De Groat ◽  
...  
Keyword(s):  
Urinary Bladder ◽  
Brain Stem ◽  
Locus Ceruleus ◽  
Ventrolateral Medulla ◽  
Reticular Nucleus ◽  
Motor Nucleus ◽  
Arterial Blood ◽  
Dorsal Motor Nucleus ◽  
The Brain ◽  
Stimulation Of

To investigate the interaction between cardiovascular (CV)-reactive areas in the brain stem and urinary bladder (UB) motility, 48 adult cats of either sex were anesthetized intraperitoneally with alpha-chloralose (40 mg/kg) and urethan (400 mg/kg). The changes of UB motility and systemic arterial blood pressure (SAP) were produced by microinjection of sodium glutamate (0.5 M, 100-200 nl) into the pressor, depressor, or vagobradycardiac areas of the brain stem. Stimulation of these CV-reactive areas increased or decreased UB motility. Areas that produced an increase in UB motility listed in decreasing order of effectiveness are locus ceruleus-parabrachial nucleus in the pons, dorsal medulla, dorsal motor nucleus of vagus, and ventrolateral medulla. Areas eliciting a decrease in UB motility listed in decreasing order are gigantocellular tegmental field, parvocellular reticular nucleus, and ambiguus nucleus. Stimulation of other pressor sites in medulla also increased UB motility. Activation of the paramedian reticular nucleus, which consistently produced depressor responses, and activation of raphe nuclei, which produced depressor or pressor responses, consistently decreased UB motility. The integrity of the vagus nerve was not essential for the UB response to brain stimulation. These findings indicate that neuronal mechanisms for controlling UB and CV functions coexist at many sites in the brain stem. At those sites that commonly produce changes in UB motility, the type of UB response (excitation or inhibition) was in the same direction as the change of SAP. However, at some sites responses were inverse. It is not known whether the responses of the UB and CV system are controlled by common or separate populations of neurons at these sites.

Effects of insulin on the cardiovascular integrating mechanisms of brain stem in cats

1993 ◽  
Vol 265 (4) ◽  
pp. E609-E616 ◽  
Author(s):  
S. W. Kuo ◽  
J. H. Hsieh ◽  
W. C. Wu ◽  
H. T. Horng ◽  
L. R. Shian ◽  
...  
Keyword(s):  
Brain Stem ◽  
Cardiovascular Responses ◽  
Serum Glucose ◽  
Ventrolateral Medulla ◽  
Reticular Nucleus ◽  
Motor Nucleus ◽  
Renal Nerve ◽  
Pressor Responses ◽  
The Brain ◽  
Stimulation Of

In 65 cats anesthetized with alpha-chloralose and urethane, the effects of insulin on cardiovascular responses to stimulation of various structures in the brain stem were studied. The threshold dose of insulin injected intravenously that produced systemic hypoglycemia was 5-10 U/kg. Subthreshold hypoglycemic doses of insulin were used intracerebroventricularly (0.25 U/kg) or intracerebrally (2 mU in 200 nl). Sixty minutes after intravenous insulin, when serum glucose concentrations decreased from 158 to 43 mg/100 ml, pressor responses to stimulation of the periaqueductal gray of midbrain (PAG), locus coeruleus (LC), dorsal medulla (DM), ventrolateral medulla (VLM), and parvocellular reticular nucleus (PVC) decreased significantly. Depressor and bradycardiac response to stimulation of paramedian reticular nucleus or dorsal motor nucleus of vagus (DMV) decreased significantly as well. Thirty minutes after intracerebroventricular insulin, pressor responses of PAG, DM, and the bradycardiac response of DMV decreased significantly. Thirty minutes after intracerebral insulin, pressor responses and renal nerve activities of LC (but not PAG), VLM, DM, and PVC decreased significantly. A similar but faster onset (5 min) of depression of cardiovascular responses on stimulating the LC, VLM, DM, and PVC was observed in another six acutely midcollicular-decerebrate cats recovered from halothane anesthesia. These findings suggest that insulin directly inhibits the vasomotor structures of the brain stem and decreases the pressor responses to stimulation.

PYY in brain stem nuclei induces vagal stimulation of gastric acid secretion in rats

1995 ◽  
Vol 268 (6) ◽  
pp. G943-G948 ◽  
Author(s):  
H. Yang ◽  
Y. Tache
Keyword(s):  
Acid Secretion ◽  
Brain Stem ◽  
Gastric Acid Secretion ◽  
Gastric Acid ◽  
Serotonin Receptor ◽  
Peptide Yy ◽  
Motor Nucleus ◽  
Dorsal Motor Nucleus ◽  
Raphe Pallidus ◽  
Stimulation Of

The influence of peptide YY (PYY) microinjected into brain stem nuclei on gastric acid secretion (GAS) was investigated in urethan-anesthetized rats with gastric cannula. PYY (30-200 ng) microinjected into the dorsal motor nucleus of the vagus (DMN) induces a dose-related and vagal-dependent stimulation of GAS (net increase from 13 +/- 4 to 59 +/- 12 mumol/90 min). PYY (200 ng) injected intravenously intracisternally into sites adjacent to the DMN had no effect. GAS induced by PYY into the DMN was potentiated by coinjection of thyrotropin-releasing hormone (TRH, 30 ng) or the serotonin receptor (5-HT2) agonist (+/-)-1-(4-methyl-1-piperazinyl)-pyrrolo(1,2-a)quinoxaline (357 ng) and by microinjection of kainic acid (1 ng) into the raphe pallidus. Prepro-TRH-(160-169) (200 ng into the DMN) did not influence the stimulatory effect of PYY. PYY (200 ng) microinjected into the raphe pallidus, raphe obscurus, and nucleus ambiguous also increased GAS, although the response was of shorter duration than that in the DMN. These results indicate that PYY acts in brain stem nuclei involved in the vagal regulation of GAS and that PYY action in the DMN is potentiated by TRH or 5-HT2 receptor agonist acting at this site.

Predominance of vagal bradycardia mechanism in the brain stem of turtles

1988 ◽  
Vol 140 (1) ◽  
pp. 405-420 ◽  
Author(s):  
J. H. Hsieh ◽  
C. M. Pan ◽  
J. S. Kuo ◽  
C. Y. Chai
Keyword(s):  
Blood Pressure ◽  
Brain Stem ◽  
Pressor Response ◽  
Inhibitory Response ◽  
Cardiac Contraction ◽  
Vagus Nerves ◽  
Arterial Blood ◽  
Vagal Bradycardia ◽  
The Brain ◽  
Stimulation Of

Cardiovascular parameters of spontaneously breathing pond turtles (Cyclemys flavomarginata) anaesthetized with chloralose (4 mg 100 g-1) and urethane (40 mg 100 g-1), were examined during exploratory electrical stimulation of the brain stem. Turtles exhibited a low mean systemic arterial blood pressure (MSAP, average 25 mmHg) and slow heart rate (average 24 beats min-1). Upon stimulation, pressor (sympathetic), depressor (sympathetic inhibition), bradycardia and hypotensive (vagal) responses were elicited from regions of the brain stem extending from the hypothalamus to the medulla, principally in the medial region. The pressor response appeared after a longer latency than did the bradycardia and hypotensive responses. It developed rather slowly, and rarely attained a magnitude double its resting value. In contrast, stimulation of many points in the brain stem produced marked slowing or even cessation of the heart beat, and thus resulted in an immediate fall of the blood pressure even to zero. This cardio-inhibitory response depended on the integrity of the vagus nerves and was particularly marked upon stimulation in the caudal medulla, the areas of the ambiguus, solitary and dorsomotor nuclei of the vagus and the midline structures. When such an area was stimulated continuously the heart stopped beating throughout the stimulation. The longest period of cardiac arrest before the appearance of escape was 35 min. With continuous stimulation of the peripheral end of the cut vagus, the earliest escape beat occurred even later (65 min). Epinephrine given intravenously produced an increase of MSAP and force of cardiac contraction, although the slope of pressor rise was shallow. Reflex bradycardia, however, was not observed. These experiments show that a very prominent vagal bradycardia can be evoked from the turtle brain stem, which may contribute to its well-known capacity for tolerating anoxia.

scholarly journals Vagally mediated effects of brain stem dopamine on gastric tone and phasic contractions of the rat

2017 ◽  
Vol 313 (5) ◽  
pp. G434-G441 ◽  
Author(s):  
L. Anselmi ◽  
L. Toti ◽  
C. Bove ◽  
R. A. Travagli
Keyword(s):  
Receptor Antagonist ◽  
Brain Stem ◽  
Sch 23390 ◽  
Systemic Administration ◽  
Membrane Properties ◽  
Receptor Subtype ◽  
Motor Nucleus ◽  
Gastric Tone ◽  
Dorsal Motor Nucleus ◽  
The Brain

Dopamine (DA)-containing fibers and neurons are embedded within the brain stem dorsal vagal complex (DVC); we have shown previously that DA modulates the membrane properties of neurons of the dorsal motor nucleus of the vagus (DMV) via DA1 and DA2 receptors. The vagally dependent modulation of gastric tone and phasic contractions, i.e., motility, by DA, however, has not been characterized. With the use of microinjections of DA in the DVC while recording gastric tone and motility, the aims of the present study were 1) assess the gastric effects of brain stem DA application, 2) identify the DA receptor subtype, and, 3) identify the postganglionic pathway(s) activated. Dopamine microinjection in the DVC decreased gastric tone and motility in both corpus and antrum in 29 of 34 rats, and the effects were abolished by ipsilateral vagotomy and fourth ventricular treatment with the selective DA2 receptor antagonist L741,626 but not by application of the selective DA1 receptor antagonist SCH 23390. Systemic administration of the cholinergic antagonist atropine attenuated the inhibition of corpus and antrum tone in response to DA microinjection in the DVC. Conversely, systemic administration of the nitric oxide synthase inhibitor nitro-l-arginine methyl ester did not alter the DA-induced decrease in gastric tone and motility. Our data provide evidence of a dopaminergic modulation of a brain stem vagal neurocircuit that controls gastric tone and motility. NEW & NOTEWORTHY Dopamine administration in the brain stem decreases gastric tone and phasic contractions. The gastric effects of dopamine are mediated via dopamine 2 receptors on neurons of the dorsal motor nucleus of the vagus. The inhibitory effects of dopamine are mediated via inhibition of the postganglionic cholinergic pathway.

Δ9-Tetrahydrocannabinol selectively acts on CB1 receptors in specific regions of dorsal vagal complex to inhibit emesis in ferrets

2003 ◽  
Vol 285 (3) ◽  
pp. G566-G576 ◽  
Author(s):  
Marja D. Van Sickle ◽  
Lorraine D. Oland ◽  
Ken Mackie ◽  
Joseph S. Davison ◽  
Keith A. Sharkey
Keyword(s):  
Receptor Antagonist ◽  
Brain Stem ◽  
Area Postrema ◽  
Motor Nucleus ◽  
Cb1 Receptors ◽  
Dorsal Vagal Complex ◽  
Dorsal Motor Nucleus ◽  
Site Of Action ◽  
Fos Expression ◽  
The Brain

The aim of this study was to investigate the efficacy, receptor specificity, and site of action of Δ9-tetrahydrocannabinol (THC) as an antiemetic in the ferret. THC (0.05-1 mg/kg ip) dose-dependently inhibited the emetic actions of cisplatin. The ED50 for retching was ∼0.1 mg/kg and for vomiting was 0.05 mg/kg. A specific cannabinoid (CB)1 receptor antagonist SR-141716A (5 mg/kg ip) reversed the effect of THC, whereas the CB2 receptor antagonist SR-144528 (5 mg/kg ip) was ineffective. THC applied to the surface of the brain stem was sufficient to inhibit emesis induced by intragastric hypertonic saline. The site of action of THC in the brain stem was further assessed using Fos immunohistochemistry. Fos expression induced by cisplatin in the dorsal motor nucleus of the vagus (DMNX) and the medial subnucleus of the nucleus of the solitary tract (NTS), but not other subnuclei of the NTS, was significantly reduced by THC rostral to obex. At the level of the obex, THC reduced Fos expression in the area postrema and the dorsal subnucleus of the NTS. The highest density of CB1 receptor immunoreactivity was found in the DMNX and the medial subnucleus of the NTS. Lower densities were observed in the area postrema and dorsal subnucleus of the NTS. Caudal to obex, there was moderate density of staining in the commissural subnucleus of the NTS. These results show that THC selectively acts at CB1 receptors to reduce neuronal activation in response to emetic stimuli in specific regions of the dorsal vagal complex.

Differential control over postganglionic neurons in rat cardiac ganglia by NA and DmnX neurons: anatomical evidence

2004 ◽  
Vol 286 (4) ◽  
pp. R625-R633 ◽  
Author(s):  
Zixi (Jack) Cheng ◽  
Hong Zhang ◽  
Shang Z. Guo ◽  
Robert Wurster ◽  
David Gozal
Keyword(s):  
Brain Stem ◽  
Motor Neurons ◽  
Nucleus Ambiguus ◽  
Motor Nucleus ◽  
Sprague Dawley ◽  
Tracer Injection ◽  
Cardiac Ganglia ◽  
Dorsal Motor Nucleus ◽  
Differential Control ◽  
The Brain

In previous single-labeling experiments, we showed that neurons in the nucleus ambiguus (NA) and the dorsal motor nucleus of the vagus (DmnX) project to intrinsic cardiac ganglia. Neurons in these two motor nuclei differ significantly in the size of their projection fields, axon caliber, and endings in cardiac ganglia. These differences in NA and DmnX axon cardiac projections raise the question as to whether they target the same, distinct, or overlapping populations of cardiac principal neurons. To address this issue, we examined vagal terminals in cardiac ganglia and tracer injection sites in the brain stem using two different anterograde tracers {1,1′-dioleyl-3,3,3′,3′-tetramethylindocarbocyanine methanesulfonate and 4-[4-(dihexadecylamino)-styryl]- N-methylpyridinium iodide} and confocal microscopy in male Sprague-Dawley rats. We found that 1) NA and DmnX neurons innervate the same cardiac ganglia, but these axons target separate subpopulations of principal neurons and 2) axons arising from neurons in the NA and DmnX in the contralateral sides of the brain stem enter the cardiac ganglionic plexus through separate bundles and preferentially innervate principal neurons near their entry regions, providing topographic mapping of vagal motor neurons in left and right brain stem vagal nuclei. Because the NA and DmnX project to distinct populations of cardiac principal neurons, we propose that they may play different roles in controlling cardiac function.

scholarly journals Insulin reduces excitation in gastric-related neurons of the dorsal motor nucleus of the vagus

2012 ◽  
Vol 303 (8) ◽  
pp. R807-R814 ◽  
Author(s):  
Camille B. Blake ◽  
Bret N. Smith
Keyword(s):  
Brain Stem ◽  
Synaptic Input ◽  
Energy Homeostasis ◽  
Gastric Wall ◽  
Insulin Receptors ◽  
Excitatory Input ◽  
Motor Nucleus ◽  
Action Potential Firing ◽  
Dorsal Motor Nucleus ◽  
The Brain

The dorsal motor nucleus of the vagus (DMV) in the caudal brain stem is composed mainly of preganglionic parasympathetic neurons that control the subdiaphragmatic viscera and thus participates in energy homeostasis regulation. Metabolic pathologies, including diabetes, can disrupt vagal circuitry and lead to gastric dysfunction. Insulin receptors (IRs) are expressed in the DMV, and insulin crosses the blood-brain barrier and is transported into the brain stem. Despite growing evidence that insulin action in the brain is critical for energy homeostasis, little is known about insulin's action in the DMV. We used whole cell patch-clamp recordings in brain stem slices to identify effects of insulin on membrane and synaptic input properties of DMV neurons, including a subset of gastric-related cells identified subsequent to injection of a retrograde label into the gastric wall. Insulin application significantly reduced the frequency of spontaneous and miniature excitatory, but not inhibitory postsynaptic currents, with no change in amplitude ( P < 0.05). Insulin also directly hyperpolarized the membrane potential (−4.2 ± 1.3 mV; P < 0.05) and reduced action potential firing ( P < 0.05). Insulin effects were eliminated in the presence of a ATP-dependent K+ (KATP) channel antagonist tolbutamide (200 μM), or the phosphatidylinositol 3-kinase (PI3K) inhibitor wortmannin (100 nM), suggesting that insulin inhibition of excitatory input to gastric-related DMV neurons was mediated by KATP channels and depended on PI3K activity. Insulin regulation of synaptic input in the DMV may influence autonomic visceral regulation and thus systemic glucose metabolism.

scholarly journals Responses of neurons in the rostral ventrolateral medulla to whole body rotations: comparisons in decerebrate and conscious cats

2011 ◽  
Vol 110 (6) ◽  
pp. 1699-1707 ◽  
Author(s):  
V. J. DeStefino ◽  
D. A. Reighard ◽  
Y. Sugiyama ◽  
T. Suzuki ◽  
L. A. Cotter ◽  
...  
Keyword(s):  
Brain Stem ◽  
Body Position ◽  
Rostral Ventrolateral Medulla ◽  
Whole Body ◽  
Ventrolateral Medulla ◽  
Otolith Organs ◽  
Decerebrate Cats ◽  
Conscious Animals ◽  
The Brain ◽  
Stimulation Of

The responses to vestibular stimulation of brain stem neurons that regulate sympathetic outflow and blood flow have been studied extensively in decerebrate preparations, but not in conscious animals. In the present study, we compared the responses of neurons in the rostral ventrolateral medulla (RVLM), a principal region of the brain stem involved in the regulation of blood pressure, to whole body rotations of conscious and decerebrate cats. In both preparations, RVLM neurons exhibited similar levels of spontaneous activity (median of ∼17 spikes/s). The firing of about half of the RVLM neurons recorded in decerebrate cats was modulated by rotations; these cells were activated by vertical tilts in a variety of directions, with response characteristics suggesting that their labyrinthine inputs originated in otolith organs. The activity of over one-third of RVLM neurons in decerebrate animals was altered by stimulation of baroreceptors; RVLM units with and without baroreceptor signals had similar responses to rotations. In contrast, only 6% of RVLM neurons studied in conscious cats exhibited cardiac-related activity, and the firing of just 1% of the cells was modulated by rotations. These data suggest that the brain stem circuitry mediating vestibulosympathetic reflexes is highly sensitive to changes in body position in space but that the responses to vestibular stimuli of neurons in the pathway are suppressed by higher brain centers in conscious animals. The findings also raise the possibility that autonomic responses to a variety of inputs, including those from the inner ear, could be gated according to behavioral context and attenuated when they are not necessary.

Neurons in the dorsal motor nucleus of the vagus may integrate vagal and spinal information from the GI tract

1995 ◽  
Vol 268 (5) ◽  
pp. G780-G790 ◽  
Author(s):  
W. E. Renehan ◽  
X. Zhang ◽  
W. H. Beierwaltes ◽  
R. Fogel
Keyword(s):  
Brain Stem ◽  
Vagal Afferents ◽  
High Threshold ◽  
Motor Nucleus ◽  
Potential Contribution ◽  
Gi Tract ◽  
Dorsal Motor Nucleus ◽  
Efferent Neurons ◽  
Spinal Afferents ◽  
The Brain

Previous investigations have provided evidence that the activity of parasympathetic efferent neurons in the dorsal motor nucleus of the vagus (DMNV) may be influenced by either vagal afferent or spinal input from the gastrointestinal (GI) tract. Many questions remain, however, regarding the nature of this input and its integration by the brain stem. The present study was designed to examine one important aspect of this issue: the potential contribution of the spinal input to the brain stem in the generation of the response properties of intestine-sensitive neurons in the DMNV. Using intracellular recording and labeling techniques in adult rats, we found that ascending spinal pathways were capable of conveying both low- and high-threshold visceral information to the DMNV. We also determined that the neurons in the nucleus of the solitary tract failed to respond to intestinal distention when the vagal afferents to the brain stem had been severed, suggesting that the spinal projections terminate directly on the DMNV neurons. These data lend support to the emerging hypothesis that the spinal afferents that accompany the abdominal splanchnics are capable of responding to both innocuous and noxious stimuli. The results also suggest that the neurons in the DMNV play a larger role in the integration of visceral sensory information than was previously realized.

scholarly journals Differential organization of excitatory and inhibitory synapses within the rat dorsal vagal complex

2011 ◽  
Vol 300 (1) ◽  
pp. G21-G32 ◽  
Author(s):  
Tanja Babic ◽  
Kirsteen N. Browning ◽  
R. Alberto Travagli
Keyword(s):  
Brain Stem ◽  
Pancreatic Secretion ◽  
Firing Frequency ◽  
Inhibitory Synapses ◽  
Motor Nucleus ◽  
Glutamatergic Synapses ◽  
Dorsal Motor Nucleus ◽  
Whole Cell Patch Clamp ◽  
The Brain ◽  
Upper Gastrointestinal

The dorsal motor nucleus of the vagus (DMV) is pivotal in the regulation of upper gastrointestinal functions, including motility and both gastric and pancreatic secretion. DMV neurons receive robust GABA- and glutamatergic inputs. Microinjection of the GABAA antagonist bicuculline (BIC) into the DMV increases pancreatic secretion and gastric motility, whereas the glutamatergic antagonist kynurenic acid (KYN) is ineffective unless preceded by microinjection of BIC. We used whole cell patch-clamp recordings with the aim of unveiling the brain stem neurocircuitry that uses tonic GABA- and glutamatergic synapses to control the activity of DMV neurons in a brain stem slice preparation. Perfusion with BIC altered the firing frequency of 71% of DMV neurons, increasing firing frequency in 80% of the responsive neurons and decreasing firing frequency in 20%. Addition of KYN to the perfusate either decreased (52%) or increased (25%) the firing frequency of BIC-sensitive neurons. When KYN was applied first, the firing rate was decreased in 43% and increased in 21% of the neurons; further perfusion with BIC had no additional effect in the majority of neurons. Our results indicate that there are several permutations in the arrangements of GABA- and glutamatergic inputs controlling the activity of DMV neurons. Our data support the concept of brain stem neuronal circuitry that may be wired in a finely tuned organ- or function-specific manner that permits precise and discrete modulation of the vagal motor output to the gastrointestinal tract.

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