Vagal preganglionic projections to the enteric nervous system characterized withPhaseolus vulgaris-leucoagglutinin

Holst, M.-C.; Kelly, Joshua B.; Powley, Terry L.

doi:10.1002/(sici)1096-9861(19970428)381:1<81::aid-cne7>3.0.co;2-g

Cited by 114 publications

(78 citation statements)

References 25 publications

(32 reference statements)

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“…Previous observations have suggested that most, if not all, myenteric neurons in the stomach are contacted by vagal preganglionic terminals Holst et al, 1997), and the present results corroborate the conclusion. In addition, though, the present results for the first time indicate that virtually all of these efferent axonal projections are positive for alpha-synuclein.…”

Section: Alpha-synuclein-positive Pathways Innervating the Gutsupporting

confidence: 92%

“…Thus the Braak model suggests the general proposal that Parkinson's disease may be produced by an environmental pathogen that breaches the mucosal barrier of the gastrointestinal (GI) tract (and presumably the olfactory system as well; Hawkes et al, 2007) in susceptible individuals. Further, the model suggests that the stomach is the most likely starting point for any pathological insult to gain access to axons from the dorsal vagal complex, because of the heavy innervation of the GI tract by vagal preganglionics Holst et al, 1997).…”

Section: Introductionmentioning

confidence: 99%

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Alpha-synuclein-immunopositive myenteric neurons and vagal preganglionic terminals: Autonomic pathway implicated in Parkinson's disease?

et al. 2008

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The protein alpha-synuclein is implicated in the development of Parkinson's disease. The molecule forms Lewy body aggregates that are hallmarks of the disease, has been associated with the spread of neuropathology from the peripheral to the central nervous system, and appears to be involved with the autonomic disorders responsible for the gastrointestinal (GI) symptoms of individuals afflicted with Parkinson's. To characterize the normative expression of alpha-synuclein in the innervation of the GI tract, we examined both the postganglionic neurons and the preganglionic projections by which the disease is postulated to retrogradely invade the CNS. Specifically, in Fischer 344 and Sprague Dawley rats, immunohistochemistry in conjunction with injections of the tracer DextranTexas Red was used to determine, respectively, the expression of alpha-synuclein in the myenteric plexus and in the vagal terminals. Alpha-synuclein is expressed in a subpopulation of myenteric neurons, with the proportion of positive somata increasing from the stomach (~3%) through duodenum (proximal, ~6%; distal, ~13%) to jejunum (~22%). Alpha-synuclein is co-expressed with the nitrergic enzyme NOS or the cholinergic markers calbindin and calretinin in regionally specific patterns: ~90% of forestomach neurons positive for alpha-synuclein express NOS, whereas ~92% of corpus-antrum neurons positive for alpha-synuclein express cholinergic markers. Vagal afferent endings in the myenteric plexus and the GI smooth muscle do not express alpha-synuclein, whereas, virtually all vagal preganglionic projections to the gut express alpha-synuclein, both in axons and in terminal varicosites in apposition with myenteric neurons. Vagotomy eliminates most, but not all, alpha-synuclein-positive neurites in the plexus. Some vagal preganglionic efferents expressing alphasynuclein form varicose terminal rings around myenteric plexus neurons that are also positive for the protein, thus providing a candidate alpha-synuclein-expressing pathway for the retrograde transport of putative Parkinson's pathogens or toxins from the ENS to the CNS.

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Section: Alpha-synuclein-positive Pathways Innervating the Gutsupporting

confidence: 92%

Section: Introductionmentioning

confidence: 99%

Alpha-synuclein-immunopositive myenteric neurons and vagal preganglionic terminals: Autonomic pathway implicated in Parkinson's disease?

et al. 2008

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“…Second, the Fos expression was induced in the enteric plexuses of the stomach and duodenum but not in the jejunum, ileum, and colon, a fact that accords with the denser distribution of the vagal innervation in the upper GI tract (52). Anterograde tracing studies showed that vagal efferent terminals form a dense network encircling or making putative contact with nearly all myenteric neurons in the rat corpus and antrum (19). The profuse, widespread, and similar magnitude of Fos expression in the corpus, antral, and duodenal myenteric ganglia in response to insulin hypoglycemia is consistent with the vagal efferent innervation in these areas (19).…”

Section: Discussionmentioning

confidence: 79%

“…This caudal raphe-DVC pathway plays an important role in vagalmediated stimulation of gastric functions by cold stress (6,70,71). Peripherally, the gastric and duodenal enteric plexuses, which innervate smooth muscle/mucosal layers and play important roles in regulating gastric and duodenal secretion and motility (14, 50), receive a dense and intricate network of vagal efferent axons (2,19,77). Studies on the neuronal responses to abnormal blood glucose levels in these central vagal-…”

mentioning

confidence: 99%

Neuronal activation of brain vagal-regulatory pathways and upper gut enteric plexuses by insulin hypoglycemia

Yuan

Yang

2002

American Journal of Physiology-Endocrinology and Metabolism

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Yuan, Pu-Qing, and Hong Yang. Neuronal activation of brain vagal-regulatory pathways and upper gut enteric plexuses by insulin hypoglycemia. Am J Physiol Endocrinol Metab 283: E436-E448, 2002;10.1152/ajpendo.00538.2001.-Neuronal activation of brain vagal-regulatory nuclei and gastric/duodenal enteric plexuses in response to insulin (2 U/kg, 2 h) hypoglycemia was studied in rats. Insulin hypoglycemia significantly induced Fos expression in the paraventricular nucleus of the hypothalamus, locus coeruleus, dorsal motor nucleus of the vagus (DMN), and nucleus tractus solitarii (NTS), as well as in the gastric/duodenal myenteric/submucosal plexuses. A substantial number of insulin hypoglycemia-activated DMN and NTS neurons were choline acetyltransferase and tyrosine hydroxylase positive, respectively, whereas the activated enteric neurons included NADPH-and vasoactive intestinal peptide neurons. The numbers of Fos-positive cells in each above-named brain nucleus or in the gastric/duodenal myenteric plexus of insulin-treated rats were negatively correlated with serum glucose levels and significantly increased when glucose levels were lower than 80 mg/dl. Acute bilateral cervical vagotomy did not influence insulin hypoglycemia-induced Fos induction in the brain vagal-regulatory nuclei but completely and partially prevented this response in the gastric and duodenal enteric plexuses, respectively. These results revealed that brain-gut neurons regulating vagal outflow to the stomach/ duodenum are sensitively responsive to insulin hypoglycemia. dorsal motor nucleus of the vagus; nucleus tractus solitarii; glucose; vagus; stomach CONVERGING EVIDENCE SUGGESTS that hyper-or hypoglycemia affects gastrointestinal (GI) functions by influencing vagal-cholinergic outflow to the viscera. The involvement of upper GI tract organs in the hyperglycemia-induced delay of gastric emptying (5) corresponds to the distribution of the vagus in the GI tract (52). GI functions that are well established to be stimulated by vagal efferent activation, such as sham feeding-induced gastric acid secretion and pancreatic polypeptide release from the pancreas, were remarkably reduced during hyperglycemia (34). In contrast to hyperglycemia, insulin hypoglycemia is well established as a central vagal stimulus on upper GI functions (63,64,67). Visceral response to insulin hypoglycemia has been widely used to test vagus nerve integrity (67), especially used postoperatively to test the result of vagotomy (45). These findings established a role of the vagus nerve in mediating the regulation of GI functions by altered glucose metabolism. However, how the neurons in the brain vagal-regulatory nuclei and GI enteric plexuses respond to hypo-or hyperglycemia is still poorly understood.The medullary dorsal vagal complex (DVC) is composed of the dorsal motor nucleus of the vagus (DMN) and the nucleus tractus solitarii (NTS), which respectively contain somata of parasympathetic efferents that project to the GI tract (4, 48, 61) and neurons receiving vagal afferent i...

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“…By the use of immunoelectron microscopy, nerve fibers and varicosities immunoreactive for either vAChT or NOS were found within the circular and longitudinal muscle layers. It is likely that the majority of these fibers were nerve terminals of enteric motor neurons, and it is unlikely that vAChT immunoreactivity was caused by vagal efferent fibers because these neurons do not terminate within the muscle layers (Holst et al, 1997). vAChT immunoreactivity was associated with either the membranes or within the lumen of vesicles within varicosities.…”

Section: Morphological Relationships Between Enteric Motor Neurons Anmentioning

confidence: 99%

Interstitial Cells of Cajal Mediate Cholinergic Neurotransmission from Enteric Motor Neurons

et al. 2000

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Interstitial cells of Cajal (ICC) are interposed between enteric neurons and smooth muscle cells in gastrointestinal muscles. The role of intramuscular ICC (IC-IM) in mediating enteric excitatory neural inputs was studied using gastric fundus muscles of wild-type animals and W/W v mutant mice, which lack IC-IM. Excitatory motor neurons, labeled with antibodies to vesicular acetylcholine transporter or substance-P, were closely associated with IC-IM. Immunocytochemistry showed close contacts between enteric neurons and IC-IM. IC-IM also formed gap junctions with smooth muscle cells. Electrical field stimulation yielded fast excitatory junction potentials in the smooth muscle that were blocked by atropine. Neural responses were greatly reduced in muscles of W/W v animals. Loss of cholinergic responses in W/W v muscles seemed to be caused by the loss of close synaptic contacts between motor neurons and IC-IM, because these muscles were not less responsive to exogenous acetylcholine than were wild-type muscles. W/W v muscles also responded to excitatory nerve stimulation when the breakdown of acetylcholine was blocked by neostigmine. The density of cholinergic nerve bundles within the muscles was not significantly different in wild-type and W/W v muscles, and similar amounts of 14 [C]choline were released from preloaded wildtype and W/W v muscles in response to nerve stimulation. The impact of losing IC-IM on gastric compliance was also evaluated in intact stomachs. Pressure increased as a function of fluid volume and infusion rate in wild-type animals, but W/W v animals showed little basal tone and minimal increases in pressure with fluid infusions. These data suggest that IC-IM play a major role in receiving cholinergic excitatory inputs from the enteric nervous system in the murine fundus.

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Vagal preganglionic projections to the enteric nervous system characterized withPhaseolus vulgaris-leucoagglutinin

Cited by 114 publications

References 25 publications

Alpha-synuclein-immunopositive myenteric neurons and vagal preganglionic terminals: Autonomic pathway implicated in Parkinson's disease?

Alpha-synuclein-immunopositive myenteric neurons and vagal preganglionic terminals: Autonomic pathway implicated in Parkinson's disease?

Neuronal activation of brain vagal-regulatory pathways and upper gut enteric plexuses by insulin hypoglycemia

Interstitial Cells of Cajal Mediate Cholinergic Neurotransmission from Enteric Motor Neurons

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