Effects of portal infusion of hypotonic- and hypertonic solutions on neuronal activity in the rat dorsal motor nucleus of the vagus

The present experiment was designed to elucidate the characteristics of the response of neurons in the dorsal motor nucleus of the vagus (DMV) to stimulation of the hepatoportal area by hypotonic as well as hypertonic solutions. Responses of 81 neurons that exhibited an antidromic response to electrical stimulation of the ventral gastric vagus were recorded in the left DMV in urethane-chloralose anesthetized rats. The effects on these 81 neurons of portal infusion of hypertonic saline (3.6% NaCI) and of pure water were examined. The discharge rates of 16 neurons increased in response both to portal infusion of hypertonic saline and to that of water. Portal infusion of 0.9% NaCl produced no changes in firing rates. Their discharge rates of seven neurons increased in response to portal infusion of hypertonic saline but not to that of water. The other 58 neurons did not respond to these stimuli. Jugular infusion of water produced no response. Therefore, the responses to portal infusion of water appear to be derived from activation of the hepatoportal receptors. These results indicate that a certain fraction of DMV neurons respond similarly to portal infusions of hypertonic and hypotonic saline. It is possible that there exist some reflex arcs that mediate a similar response to both an increase and a decrease in portal blood osmolarity (or Na⁺ concentration), namely, a suppression of absorption.     

Effect of portal infusion of hypertonic saline on neurons in the dorsal motor nucleus of the vagus in the rat

Effects of hepatoportal osmo-receptive (or sodium-receptive) afferents on neurons within the dorsal motor nucleus of the vagus (DMV) were investigated electrophysiologically in urethane-chloralose anesthetized rats. Responses of 56 spontaneously active neurons to antidromic stimulation of the ventral trunk of the subdiaphragmatic vagus were recorded in the left DMV. Among them, 35 neurons were inhibited by electrical stimulation of the hepatic branch of the vagus nerve (inhibitory neurons), except two neurons that were slightly excited. Effects of portal infusion of 3.6% NaCl were examined on 26 inhibitory neurons. Sixteen neurons increased their discharge rates and one neuron decreased its discharge rate in response to portal infusion of hypertonic saline. Thirty-five DMV neurons responded to electrical stimulation of the dorsal trunk of the subdiaphragmatic vagus were inhibited by electrical stimulation of the hepatic branch of the vagus. Four neurons were excited by this stimulation. Relatively smaller number of neurons (5 out of 22 inhibitory neurons) increased their discharge rates in response to portal infusion of hypertonic saline. In conclusion, the response of DMV neuron observed in this experiment was characterized by increasing the frequency of spike discharges in response to portal infusion of hypertonic saline. However, these neurons were inhibited by electrical stimulation of the hepatic branch of the vagus nerve. These results suggest that the hepatoportal osmoreceptive afferents may be conveyed to the DMV via inhibitory synapses.     

A direct hepatic osmoreceptive afferent projection from nucleus tractus solitarius to dorsal hypothalamus

Thirty units that responded antidromically to electrical stimulation of the zona incerta (ZI) or the dorsal portion of hypothalamus were recorded in the nucleus tractus solitarii (NTS). These units were analyzed in relation to hepatoportal afferent inputs. Electrical stimulation of the hepatic branch of the vagus nerve facilitated six units (facilitatory units) and suppressed 10 units (suppressed units). Effect of the portal infusion of hypertonic saline was examined on six facilitatory and eight suppressed units. One facilitatory unit and one suppressed unit increased their discharge rates in response to portal infusion. Four facilitatory units and one suppressed unit decreased their discharge rates in response to the same stimulation. Increased or decreased discharge rates in response to portal infusion of hypertonic saline were observed in units that responded antidromically to electrical stimulation of the paraventricular hypothalamic nucleus, the lateral hypothalamic area, or the ZI. It is concluded that hepatoportal osmoreceptive signals are conveyed to the hypothalamus or the ZI directly from the NTS.     

A hepatoportal osmoreceptive afferent projection from nucleus tractus solitarius to caudal ventrolateral medulla

This study was performed to examine projection of nucleus tractus solitarii (NTS) neurons to the caudal ventrolateral medulla (cVLM) in rats. One hundred and seven neurons that responded antidromically to electrical stimulation of the cVLM were recorded within the NTS. Electrical stimulation of the hepatic branch of the vagus nerve (hepatic vagus) elicited facilitation on 62 neurons (facilitatory neurons) and suppression on 6 neurons (suppressed neurons). Effect of portal infusion of hypertonic saline was examined on 44 facilitatory and 4 suppressed neurons. Twelve facilitatory and 2 suppressed neurons showed a decrease in the discharge rate. One suppressed neuron showed an increase in the discharge rate. It is concluded that hepatoportal osmoreceptive signals are conveyed from the NTS to the cVLM. The responses are mostly characterized by the decrease in the discharge rate by portal infusion of hypertonic saline.     

Projection of nucleus tractus solitarius units influenced by hepatoportal afferent signal to parabrachial nucleus

In urethan-chloralose anesthetized rats, units in the nucleus tractus solitarius (NTS) which antidromically responded to electrical stimulation of the parabrachial nucleus (PB) were investigated for their responses to hepatic-vagal afferent signals. Among 63 NTS units examined, 25 (40%) were excited, 17 (27%) inhibited and the remaining 21 (33%) unaffected by single shock electrical stimulation of the hepatic branch of the vagus nerve. Topical application of Na+ produced an increase in discharge rate of 9 units and a decrease in 5 units. Portal infusion of hypertonic saline produced an increase in discharge rate of 3 units and a decrease in 5 units. Furthermore, 3 units responded to both topical application of Na+ and portal infusion of hypertonic saline.     

Vagal neurons and pathways to the rat's lower viscera: An electrophysiological study

The vagal pathways to the rat's pancreas are anatomically difficult to describe. A stimulation/recording technique has been used on various segments of the vagus to trace vagal pathways to the lower viscera, and a microelectrode recording technique to locate vagal neurons of origin in the brain stem's dorsal motor nucleus (DMX). The two main pathways (right cervical vagus to dorsal celiac branch and left cervical vagus to ventral celiac branch) are supplemented by two accessory ones where each cervical vagus gives some fibers to its contralateral homologue at the diaphragmatic level. These pathways consist almost exclusively of C-fibers. Neurons of origin of the dorsal vagal trunk fibers have been identified by the collision test and occupy the caudal half of the DMX; those of the dorsal celiac branch fibers originate from the medial part of that area.     

Functional effects and characteristics of cecum-projecting neurons in the dorsal motor nucleus of the vagus of rats

Preganglionic neurons in the dorsal motor nucleus of the vagus (DMV) innervate most of the gastrointestinal tract; with the stomach and the cecum/proximal colon having a greater proportion of vagal input. Cecum-projecting neurons have been thought to be distinct from other preganglionic neurons due to their location within the DMV, but it is unknown whether these neurons innervate the cecum exclusively or what effect their activation has on cecal motor activity. Therefore, we investigated the extent of coinnervation of cecum and stomach by vagal neurons, their neurochemistry, and the effect of DMV stimulation on intracecal and intragastric volumes. Fluorescent retrograde tracers injected into the serosa of the cecum and stomach revealed that in the DMV 49+/-5% CTB-labeled cecum-projecting neurons also innervated the stomach. Immunocytochemical staining for nitric oxide (NO) synthase and tyrosine hydroxylase indicated that only 3+/-1% and 4+/-1% of cecum-projecting neurons contained these markers, respectively. In anesthetized rats gastric and cecal volumes were measured by prototypic miniaturized dual barostats that were developed for use in rodents. Microinjection of l-glutamate into the DMV increased gastric contractile activity and tone, and reduced on-going cecum contractile activity (2.6+/-0.7 contractions/2 min after injection versus 8.2+/-0.4 contractions/2 min before injection, N = 5). The barostat was able to detect decreases (-0.88+/-0.13 ml) and increases (0.25+/-0.05 ml) in cecum volume in response to carbachol and sodium nitroprusside, respectively. In summary, cecum-projecting neurons are not an entirely exclusive population within the DMV because a percentage of these also innervate the stomach. Central vagal stimulation can modulate both gastric and cecum contractile activity. Together, these data support a role of the vagus in neural reflexes involving gastric and large bowel motor function, such as the immediate phase of the gastrocolonic reflex.     

Plasticity of vagal brainstem circuits in the control of gastric function

Background Sensory information from the viscera, including the gastrointestinal (GI) tract, is transmitted through the afferent vagus via a glutamatergic synapse to neurons of the nucleus tractus solitarius (NTS), which integrate this sensory information to regulate autonomic functions and homeostasis. The integrated response is conveyed to, amongst other nuclei, the preganglionic neurons of the dorsal motor nucleus of the vagus (DMV) using mainly GABA, glutamate and catecholamines as neurotransmitters. Despite being modulated by almost all the neurotransmitters tested so far, the glutamatergic synapse between NTS and DMV does not appear to be tonically active in the control of gastric motility and tone. Conversely, tonic inhibitory GABAergic neurotransmission from the NTS to the DMV appears critical in setting gastric tone and motility, yet, under basal conditions, this synapse appears resistant to modulation. Purpose Here, we review the available evidence suggesting that vagal efferent output to the GI tract is regulated, perhaps even controlled, in an ‘on‐demand’ and efficient manner in response to ever‐changing homeostatic conditions. The focus of this review is on the plasticity induced by variations in the levels of second messengers in the brainstem neurons that form vago‐vagal reflex circuits. Emphasis is placed upon the modulation of GABAergic transmission to DMV neurons and the modulation of afferent input from the GI tract by neurohormones/neurotransmitters and macronutrients. Derangement of this ‘on‐demand’ organization of brainstem vagal circuits may be one of the factors underlying the pathophysiological changes observed in functional dyspepsia or hyperglycemic gastroparesis.     

Oxytocin-immunoreactive innervation of identified neurons in the rat dorsal vagal complex

Background Oxytocin (OXT) has been implicated in reproduction and social interactions and in the control of digestion and blood pressure. OXT‐immunoreactive axons occur in the dorsal vagal complex (DVC; nucleus tractus solitarius, NTS, dorsal motor nucleus of the vagus, DMV, and area postrema, AP), which contains neurons that regulate autonomic homeostasis. The aim of the present work is to provide a systematic investigation of the OXT‐immunoreactive innervation of dorsal motor nucleus of the vagus (DMV) neurons involved in the control of gastrointestinal (GI) function. Methods We studied DMV neurons identified by (i) prior injection of retrograde tracers in the stomach, ileum, or cervical vagus or (ii) induction of c‐fos expression by glucoprivation with 2‐deoxyglucose. Another subgroup of DMV neurons was identified electrophysiologically by stimulation of the cervical vagus and then juxtacellularly labeled with biotinamide. We used two‐ or three‐color immunoperoxidase labeling for studies at the light microscopic level. Key Results Close appositions from OXT‐immunoreactive varicosities were found on the cell bodies, dendrites, and axons of DMV neurons that projected to the GI tract and that responded to 2‐deoxyglucose and juxtacellularly labeled DMV neurons. Double staining for OXT and choline acetyltransferase revealed that OXT innervation was heavier in the caudal and lateral DMV than in other regions. OXT‐immunoreactive varicosities also closely apposed a small subset of tyrosine hydroxylase‐immunoreactive NTS and DMV neurons. Conclusions & Inferences Our results provide the first anatomical evidence for direct OXT‐immunoreactive innervation of GI‐related neurons in the DMV.     

Effects of lateral hypothalamic stimulation on medulla oblongata and gastric vagal neural responses

Recordings were made of neural activity in the medial to lateral region of the dorsal nucleus of the vagus in the medulla oblongata (NDV), and from the gastric branch of the vagal nerve (gastric vagus) in rats. Gastric acid secretion following lateral hypothalamic (LHA) stimulation was observed, and NDV neurons were identified by stimulation of the peripheral end of the gastric vagus. NDV-neurons responded to LHA stimulation with latencies of about 5 msec, and about 6.5 msec to the peripheral stimulation of the gastric vagus. Out of 274 NDV neurons, which were located by their spontaneous discharge, 186 (67.9%) responded to LHA stimulation. Gastric acid secretion (with either short or long latency) occurred in 8.6% (16/186) of these cases. These 16 neurons were considered to be ‘gastric secretory’ neurons and are discussed as such. The results imply that some LHA neurons, which are either concerned with or directly control gastric acid secretion, communicated by at least one path (probably polysynaptic) to the medulla oblongata and then via the vagus to the oxyntic cells of gastric glands.     

GABA receptors in the dorsal motor nucleus of the vagus influence feline lower esophageal sphincter and gastric function

Gamma-aminobutyric acid (GABA) antagonist (bicuculline methiodide, BIC; picrotoxin, PIC) or agonist (muscimol, MUS) microinjections were made into the dorsal motor nucleus of the vagus nerve (DMV), and effects on lower esophageal sphincter pressure (LESP), gastric motility, and gastric acid secretion were determined in chloralose-anesthetized cats. Right or left DMV sites were microinjected with BIC, PIC, MUS, or isotonic saline (140 nl) through a glass micropipette having a tip diameter of 15–21 μm. Esophageal body, LESP, and gastric fundic pressures were measured manometrically. Circular smooth muscle contractions of the antrum and pylorus were recorded with strain-gauge force transducers. Gastric acid secretion was measured every 15 min through a gastric cannula and titrated to pH 7.0. DMV microinjection sites were verified histologically. Direct BIC microinjections (0.275 or 0.550 nmol) into the DMV primarily produced a decrease in LESP (71% of all sites tested), with mean LESP changing from 23.2 ± 1.7 mmHg to 3.7 ± 0.7 mmHg (p < 0.01). Tonic LESP increases and phasic LESP contractile activity occurred less frequently. BIC-induced LESP responses were abolished by vagotomy or by microinjections of MUS (0.5 to 10 nmol) into the DMV. Direct PIC microinjection (0.232 nmol) into the DMV produced a pattern of responses similar to those observed with BIC (which were also abolished by vagotomy or by MUS microinjections into the DMV). The antrum and pylorus were also responsive to DMV microinjections of both GABA antagonists. Microinjections of BIC or PIC into the DMV produced increases in gastric circular muscle activity that occurred less frequently than LESP effects, but also were eliminated by vagotomy. The high (0.550 nmol) dose of BIC increased gastric motility significantly more often than the low dose of BIC (p < 0.05). In addition, BIC (0.550 nmol) microinjections into the DMV increased gastric secretary volume (from 0.6 ± 0.2 to 6.0 ± 2.5 ml/15 min; p < 0.01) and total titratible acid (from 34.4 ±8.9 to 86.0 ± 19.1 mEq/15 min; p < 0.01), and decreased gastric pH (from 4.63 ± 0.44 to 3.50 ± 0.49; p < 0.05). Vagotomy also eliminated the gastric secretory effects of DMV BIC. Direct microinjections of MUS into the DMV also blocked BIC- or PIC-induced changes in gastric motility and/or gastric acid secretion. Isotonic saline microinjected into the DMV did not increase basal or decrease stimulated gastric esophageal motility or gastric secretion. These data indicate that LESP, gastric motility, and gastric secretion are influenced by a tonic DMV inhibition mediated by GABA_A receptor stimulation of the DMV. Because disinhibition of these receptors clearly activates the upper gut, future work should focus on identifying the nuclei providing this synaptic input to the DMV that might be involved in the functional regulation of upper gut motor and secretory function.     

Induction of apoptosis by thrombin in the cultured neurons of dorsal motor nucleus of the vagus

Background A previous study demonstrated the presence of protease‐activated receptor (PAR) 1 and 2 in the dorsal motor nucleus of vagus (DMV). The aim of this study is to characterize the effect of thrombin on the apoptosis of DMV neurons. Methods The dorsal motor nucleus of vagus neurons were isolated from neonatal rat brainstems using micro‐dissection and enzymatic digestion and cultured. Apoptosis of DMV neurons were examined in cultured neurons. Apoptotic neuron was examined by TUNEL and ELISA. Data were analyzed using anova and Student’s t‐test. Key Results Exposure of cultured DMV neurons to thrombin (0.1 to 10 U mL^?1) for 24 h significantly increased apoptosis. Pretreatment of DMV neurons with hirudin attenuated the apoptotic effect of thrombin. Similar induction of apoptosis was observed for the PAR1 receptor agonist SFLLR, but not for the PAR3 agonist TFRGAP, nor for the PAR4 agonist YAPGKF. Protease‐activated receptors 1 receptor antagonist Mpr(Cha) abolished the apoptotic effect of thrombin, while YPGKF, a specific antagonist for PAR4, demonstrated no effect. After administration of thrombin, phosphorylation of JNK and P38 occurred as early as 15 min, and remained elevated for up to 45 min. Pretreatment of DMV neurons with SP600125, a specific inhibitor for JNK, or SB203580, a specific inhibitor for P38, significantly inhibited apoptosis induced by thrombin. Conclusions & Inferences Thrombin induces apoptosis in DMV neurons through a mechanism involving the JNK and P38 signaling pathways.     

Units in tegmental nuclei responding to stimulation of gastric vagal and greater splanchnic fibers in the cat

The response of neurons in the ventral and dorsal tegmental nuclei during electrical stimulation of the gastric vagal fibers which serve the proximal stomach and the left greater splanchnic fibers were evaluated in chloralose-anesthetized cats. The mean latency of 181 gastric vagally evoked unitary responses recorded in the tegmental nuclei was 352.2 ms, whereas the latency of the left greater splanchnic-evoked tegmental response was significantly less (63.2 ms). The unitary responses to the gastric vagal and greater splanchnic fibers stimulation were bilaterally distributed in the ventral and dorsal tegmental nuclei. Convergence of the gastric vagal input from the proximal stomach and the left greater splanchnic input was observed in 151 units (83 percent). Stimulation of the greater splanchnic nerve usually resulted in a short latency excitation followed by an inhibitory effect on gastric vagally evoked responses. The results suggested that some convergent splanchnic inhibition of gastric vagally evoked responses was mediated via an interneuron. Projections from the nucleus tractus solitarius and the parabrachial nucleus to the tegmental nuclei were also identified electrophysiologically by direct microstimulation of the two former areas. The significant number of gastric vagal and splanchnic evoked unitary responses recorded in the ventral and dorsal tegmental nuclei suggested that they may serve as an important pontine site for processing of visceral information between the nucleus tractus solitarius and forebrain sites.     

Alterations in TH- and ChAT-immunoreactive neurons in the DMV and gastric dysmotility in an LPS-induced PD rat model

To study movement disorder in Parkinson's disease (PD), an animal model of PD can be created by injecting lipopolysaccharide (LPS) into the substantia nigra of rats. In addition to body movement disorders, patients with PD often experience gastrointestinal (GI) dysfunction, such as gastroparesis. However, the underlying mechanism of these disorders remains unclear. The dorsal motor nucleus of vagus (DMV) is a well-known visceral nucleus that regulates GI function. The present study investigated alterations in DMV neurons and gastric motility in rats with LPS-induced PD (LPS-PD rats). Gastric motility was recorded using a strain gauge force transducer in vivo. The distributions of tyrosine hydroxylase (TH)- and choline acetyltransferase (ChAT)-positive neurons in the DMV were determined using immunofluorescence and confocal laser microscopy. Our results indicated that in LPS-PD rats, the number of neurons in the substantia nigra, including neurons with TH immunoreactivity, was markedly reduced, although glial cell proliferation was clearly observed. However, enhanced TH immunoreactivity and decreased ChAT immunoreactivity were found in the DMV. Furthermore, weakened gastric motility was recorded in anesthetized LPS-PD rats. In conclusion, rats with LPS-induced PD exhibited gastric dysmotility with an alteration in DMV neurons. This PD model may be used to study autonomic nervous system disorders that are often observed in patients with early-stage PD.     

Representation of the cecum in the lateral dorsal motor nucleus of the vagus nerve and commissural subnucleus of the nucleus tractus solitarii in rat.

Motor fibers of the accessory celiac and celiac vagal branches are derived from the lateral columns of the dorsal motor nucleus of the vagus nerve. These branches also contain sensory fibers that terminate within the nucleus of the tractus solitarii. This study traces the innervation of the intestines by using the tracer cholera toxin-horseradish peroxidase. In 53 rats, the tracer was injected into either the stomach, duodenum, jejunum, terminal ileum, cecum, or ascending colon. With all cecal injections, prominent retrograde labeling of cell bodies occurred bilaterally in the lateral columns of the dorsal motor nucleus of the vagus nerve above, at, and below the level of the area postrema. Dendrites of laterally positioned neurons projected medially and rostrocaudally within the dorsal motor nucleus of the vagus nerve and dorsomedially into both the medial subnucleus and parts of the commissural subnucleus of the nucleus of the tractus solitarii. Sensory terminal labeling occurred in the dorsolateral commissural subnucleus at the level of the rostral area postrema and the medial commissural subnucleus caudal to the area postrema. Additionally, there was sensory terminal labeling within a small confined area of the dorsomedial zone of the nucleus of the tractus solitarii immediately adjacent to the fourth ventricle at a level just anterior to the area postrema. Stomach injections labeled motoneurons of the medial column of the entire rostrocaudal extent of the dorsal motor nucleus of the vagus nerve and a sensory terminal field primarily in the subnucleus gelatinosus, with less intense labeling extending caudally into the medial and ventral commissural subnuclei. Dendrites of gastric motoneurons project rostrocaudally and mediolaterally within the dorsal motor nucleus of the vagus nerve and dorsolaterally within the nucleus of the tractus solitarii. They are most pronounced at the level of the rostral area postrema where many dendrites course dorsolaterally terminating primarily within the subnucleus gelatinosus. Injections of the duodenum labeled a small number of the cells within the medial aspects of the dorsal motor nucleus of the vagus nerve. Jejunal, ileal, and ascending colon injections labeled cells sparsely within the lateral aspects of the dorsal motor nucleus of the vagus nerve bilaterally. No afferent terminal labeling was evident after injection of these areas of the bowel.(ABSTRACT TRUNCATED AT 400 WORDS)     

Vagal motor neurons in rats respond to noxious and physiological gastrointestinal distention differentially

Low-pressure gastrointestinal distention modulates gastrointestinal function by a vago-vagal reflex. Noxious visceral distention, as seen in an obstruction of the gastrointestinal tract, causes abdominal pain, vomiting and affective changes. Using single neuron recording and intracellular injection techniques, we characterized the neuronal responses of neurons in the dorsal motor nucleus of the vagus (DMNV) to low- and high-pressure distensions of stomach and duodenum. Low-pressure gastric distention inhibited the mean activity of the DMNV neurons whereas high-pressure gastric distention excited many neurons. Of 47 DMNV neurons, low-pressure gastric distention inhibited 39, excited four, and did not affect four neurons. High-pressure gastric distention inhibited 26, excited 20, and left one unaffected. Thirteen of the 39 DMNV neurons inhibited by low-pressure distention of the stomach reversed their response to excitation during high-pressure gastric distention. Among 47 DMNV neurons, low-pressure duodenal distention inhibited 30, excited 10, and did not affect the remaining seven neurons. High-pressure distention of the duodenum inhibited 25 and excited 22 neurons. Eight DMNV neurons inhibited by low-pressure duodenal distention were excited in early response to high-pressure distention of the duodenum. High-pressure duodenal distention caused an early excitation and late inhibition in the mean activity of the DMNV neurons while low-pressure duodenal distention only produced late inhibition. These results suggest that different reflexes are present between physiological distention and noxious stimulation of gastrointestinal tract.     

Central injection of hypertonic saline activates angiotensin II-sensitive neurons in the anterior hypothalamic area of rats

We have previously reported that microinjection of angiotensin II into the anterior hypothalamic area (AHA) produces pressor responses and that angiotensin II-sensitive neurons in the AHA are tonically activated by endogenous angiotensins in rats. Central injection of hypertonic saline causes pressor responses via release of angiotensins in brain. In this study, we examined whether angiotensin II-sensitive neurons in the AHA are responsive to intracerebroventricular injection of hypertonic saline and whether endogenous angiotensins in the AHA are involved in the central hypertonic saline-induced pressor response. Male Wistar rats were anesthetized and artificially ventilated. Extracellular potentials were recorded from single neurons in the AHA. Intraventricular injection of hypertonic saline increased the neural activity of angiotensin II-sensitive neurons, whereas pressure application of hypertonic saline onto angiotensin II-sensitive neurons themselves did not affect their neural activities. The intraventricular hypertonic saline-induced increase of unit activity of AHA neurons was inhibited by pressure application of the angiotensin AT1 receptor antagonist losartan onto the same neurons. The hypertonic saline-induced increase of unit firing was also blocked by intraventricular injection of the amiloride-sensitive sodium channel blocker benzamil. In conscious rats, intraventricular injection of hypertonic saline produced pressor responses, and the hypertonic saline-induced pressor response was inhibited by bilateral microinjection of losartan into the AHA. Repeated intraventricular injection of hypertonic saline caused an increase in the release of angiotensins in the AHA of anesthetized rats. These findings indicate that intracerebroventricular injection of hypertonic saline increases neural activity of angiotensin II-sensitive neurons trans-synaptically via endogenous angiotensins in the AHA. In addition, these findings also indicate that the intracerebroventricular injection of hypertonic saline produces a pressor response at least partly via release of angiotensins in the AHA.     

迷走神经参与胃伤害性信息向下丘脑的传递

目的　 研究迷走神经是否参与胃伤害性信息向下丘脑室旁核的传递。 方法　 检测下列条件下c Fos蛋白在孤束核及下丘脑室旁核的表达 :①胃内注入福尔马林引起伤害性刺激 ;②福尔马林刺激结合双侧膈下迷走神经切断术。结果　胃内注入福尔马林引起的伤害性刺激可以诱导c Fos蛋白在孤束核和下丘脑室旁核等脑区的表达 ,但在胸段脊髓的I,V ,VII和X层无明显表达。胃内注入生理盐水的对照组则仅有极少量的表达 ,双侧膈下迷走神经切断术可以减少c Fos蛋白在这些部位的表达。 结论　 该研究结果表明 ,迷走神经参与了胃内脏伤害性信息向孤束核及下丘脑室旁核的传递     

Distribution of bombesin-like immunoreactivity in the nucleus of the solitary tract and dorsal motor nucleus of the rat and human: Colocalization with tyrosine hydroxylase

Bombesin is a peptide neurotransmitter/neuromodulator with important autonomic and behavioral effects that are mediated, at least in part, by bombesin-containing neurons and nerve terminals in the nucleus of the solitary tract (NTS) and the dorsal motor nucleus of the vagus (DMV). The distribution of bombesin-like immunoreactive nerve terminals/fibers and cell bodies in relation to a viscerotopically relevant subnuclear map of this region was studied by using an immunoperoxidase technique. In the rat, bombesin fiber/terminal staining was heavy in an area that included the medial subnucleus of the NTS and the DMV over their full rostral-caudal extent. Distinctly void of staining were the gelatinous, central, and rostral commissural subnuclei and the periventricular area of the NTS, regions to which gastric, esophageal, cecal, and colonic primary afferents preferentially project. The caudal commissural and dorsal subnuclei had light bombesin fiber/terminal staining, as did the intermediate, interstitial, ventral, and ventrolateral subnuclei. With colchicine pretreatment, numerous cell bodies were stained in the medial and dorsal subnuclei, with fewer neurons in the caudal commissural, intermediate, interstitial, ventral, and ventrolateral subnuclei. Bombesin-like immunoreactive neurons were found in numerous other areas of the brain, including the ventrolateral medulla, the parabrachial nucleus, and the medial geniculate body. In the human NTS/DMV complex, the distribution of bombesin fiber/terminal staining was very similar to the rat. In addition, occasional bombesin-like immunoreactive neurons were labeled in a number of subnuclei, with clusters of neurons labeled in the dorsal and ventrolateral subnuclei. Double immunofluorescence studies in rat demonstrated that bombesin colocalizes with tyrosine hydroxylase in neurons in the dorsal subnucleus of the NTS. Bombesin does not colocalize with tyrosine hydroxylase in any other location in the brain. In conclusion, the distribution of bombesin in the NTS adheres to a viscerotopically relevant map. This is the anatomical substrate for the effects of bombesin on gastrointestinal function and satiety and its likely role in concluding a meal. The anatomic similarities between human and rat suggest that bombesin has similar functions in the visceral neuraxis of these two species. Bombesin coexists with catecholamines in neurons in the dorsal subnucleus, which likely mediate, in part, the cardiovascular effects of bombesin. © 1996 Wiley-Liss, Inc.     

Gastric vagal fibres distribution and acid secretion induced by portal infusion of D-glucose

The vagal glucose signal pathway relevant to hepatic portal control of gastric acid secretion was examined in bilaterally adrenalectomized rats. The decrease in acid output after portal glucose injection was blocked by section of the hepatic branch which originates in the ventral vagus trunk below the diaphragm. After cervical vagotomy, the reduction in acid output was the same whether the section had been done on the right or the left side. The acid response was strongly inhibited by prior section of the dorsal vagus trunk at the celiac level. These results suggest that the hepatic glucose signal evoking an inhibitory action on the secretion of gastric acid has a specific pathway from the liver to the stomach, and that there is functional laterality in this pathway.