Sources of anterior gastric vagal efferent discharge in rats: an electrophysiological study.
ABSTRACT The source of vagal efferent discharge (VED) in the anterior branch of the gastric vagus was investigated in urethane-chloralose anesthetized rats using successive and selective vagal cuts. After cutting the right cervical vagus, the basal VEDs were increased in 15 out of 21 cases by 4-53% (median 18%). After both cervical vagi were cut, VEDs were reduced by 10-95% (median 90%) in 14 of 17 experiments and a subcervical basal VED was observed in all rats. Additional cut of the distal end of the anterior gastric branch did not induce a consistent effect. A small segment of subdiaphragmatic anterior gastric vagus (4-5 mm) was further isolated by a fourth cut at the proximal end of the anterior gastric vagus; abolition of the subcervical VED occurred in only 4 of 14 successful cuts whereas in the other 10 experiments, the VED was reduced by 38-94% (median 87%). Histological examination revealed the presence of neurons in a paraganglion lying within the isolated nerve segment. These findings indicate that the stomach not only receives VED descending directly from medullary vagal motor neurons (about 90%), but also (approximately 10%) from neural elements located between subcervical to upper abdomen levels (the 'subcervical VED') and/or between the bifurcation of the accessory celiac branch to the gastro-esophageal junction (the 'residual VED'). In rats there is little crossed gastric vagal innervation, in agreement with anatomical observations, although there is a robust inhibitory influence from contralateral vagal afferents on medullary vagal motor neurons.
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ABSTRACT: Intravenous cholecystokinin octapeptide (CCK-8) elicits vago-vagal reflexes that inhibit phasic gastric contractions and reduce gastric tone in urethane-anaesthetized rats. A discrete proximal subdivision of the ventral gastric vagus nerve (pVGV) innervates the proximal stomach, but the fibre populations within it have not been characterized previously.We hypothesized that I.V. CCK-8 injection would excite inhibitory efferent outflow in the pVGV, in contrast to its inhibitory effect on excitatory efferent outflow in the distal subdivision (dVGV), which supplies the distal stomach. In each VGV subdivision, a dual-recording technique was used to record afferent and efferent activity simultaneously, while also monitoring intragastric pressure (IGP). CCK-8 dose dependently (100-1000 pmol kg(-1), I.V.) reduced gastric tone, gastric contractile activity and multi-unit dVGV efferent discharge, but increased pVGV efferent firing. Single-unit analysis revealed a minority of efferent fibres in each branch whose response differed in direction from the bulk response. Unexpectedly, efferent excitation in the pVGV was significantly shorter lived and had a significantly shorter decay half-time than did efferent inhibition in the dVGV, indicating that distinct pathways drive CCK-evoked outflow to the proximal vs. the distal stomach. Efferent inhibition in the dVGV began several seconds before, and persisted significantly longer than, simultaneously recorded dVGV afferent excitation.Thus, dVGV afferent excitation could not account for the pattern of dVGV efferent inhibition. However, the time course of dVGV afferent excitation paralleled that of pVGV efferent excitation. Similarly, the duration of CCK-8-evoked afferent responses recorded in the accessory celiac branch of the vagus (ACV) matched the duration of dVGV efferent responses. The observed temporal relationships suggest that postprandial effects on gastric complicance of CCK released from intestinal endocrine cells may require circulating concentrations to rise to levels capable of exciting distal gastric afferent fibres, in contrast to more immediate effects on distal gastric contractile activity mediated via vago-vagal reflexes initiated by paracrine excitation of intestinal afferents.The Journal of Physiology 11/2010; 589(Pt 2):371-93. · 4.38 Impact Factor
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ABSTRACT: Our previous studies indicated that in rats about 10% of ventral gastric vagal efferent discharges do not originate from supracervical neural elements. To determine the origin of these efferent activities, an in vitro subdiaphragmatic vagus nerve-esophagus preparation was used. Action potentials with the same amplitude and waveform, and behaving 'all or none' characteristic are considered to be recorded from a nerve fiber and defined as an unit activity. Because these centrifugal unit activities were recorded from the proximal cut end of the ventral gastric vagal strands, they are ostensibly considered to be efferent activities. However, about 50% of unit action potential samples (21 out of 40) behave like unit activities recorded from mechanoreceptive afferent fibers. They have spot-like or diffuse mechanoreceptive fields on the subdiaphragmatic esophagus. When these receptive fields were stimulated the sensory nerve terminals in the fields generate afferent unit action potentials. These afferent potentials not only propagate orthodromically to the central nerve system, but also can be transmitted centrifugally to the gastric branches of the same vagal afferent neuron. Together with the efferent discharges of gastric vagal motor neurons, these centrifugal sensory potentials can be intercepted from the proximal cut end of gastric vagal nerve strands at gastroesophageal junction. Three types of mechanoresponsive centrifugal afferent unit activities were observed: rapidly adapting (n = 8), with or without after-discharge; slowly adapting (n = 8), with or without after-discharge, and initial high frequency followed by a plateau, with long-lasting after-discharge (n = 5). Of the tested units (n = 24), 25% were either activated or inhibited by esophageal inflation and 23% (n = 22) by esophageal deflation. It is evident that not all centrifugal unit action potentials recorded from the proximal cut end of gastric vagal nerve strands are generated from the vagal motor neurons, the recorded centrifugal unit activities may contain antidromic unit action potentials generated from the esophageal collateral branches of the gastric vagal afferent nerve fibers. These results suggest that gastric vagal afferent neurons possess collateral branches innervating the esophagus, activation of esophageal terminals may exert an effect on the gastric terminals via collateral reflex, analogous to the 'axon reflex' mechanism.Journal of the Autonomic Nervous System 05/1995; 52(2-3):83-97.
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ABSTRACT: The influence of intracisternal (ic) TRH and the stable TRH analog, RX 77368, on gastric vagal efferent discharge (GVED) was investigated in urethane-anesthetized rats. Consecutive IC injections of TRH (3, 30, and 300 ng) at 60 min intervals stimulated dose dependently multi-unit GVED with a peak increase of 90 +/- 21%, 127 +/- 18% and 145 +/- 16% respectively. In two separate studies, IC injection of RX 77368 at 1.5 or 15 ng stimulated multi-unit GVED by 142 +/- 24% and 244 +/- 95% respectively. Saline injection IC had no effect on GVED. RX 77368 (1.5 ng, ic) action was long lasting (84 +/- 13 min) compared with TRH (3 ng: 44 +/- 7 min). Single-unit analysis also showed that 13 of 13 units responded to ic RX 77368 (1.5 ng) by an increase in activity. These data indicate that low doses of TRH injected ic stimulate vagal efferent outflow to the rat stomach and that RX 77368 action is more potent than TRH.Peptides 02/1997; 18(2):213-9. · 2.52 Impact Factor