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Results for “MYENTERIC PLEXUS”

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PubMed1993

Age-induced nerve cell loss in the myenteric plexus of the small intestine in man.

We examined the number of nerve cells of the myenteric plexus and the thickness of the smooth muscle in the small intestine in autopsy material of 6 young and 6 old persons. Neurons in the myenteric plexus have been visualised by a nonhistochemical method (Giemsa) in laminar preparations of the muscularis externa. Significant reductions of at least 34% in the number of neurons in the ganglia of the myenteric plexus of the old subjects were recorded in all regions of the small intestine, especially in the duodenum where the number of neurons decreased by over 38%. However, there was no significant correlation between nerve cell count and thickness of intestinal smooth muscle since no difference was found in thickness of intestinal smooth muscle between young and old subjects. The decrease in the neuron density with age could affect the potential of the enteric nervous system to influence control over several small intestinal functional parameters.

Adult↗

PubMed2000

[Histochemical study on the nitric oxide synthase in the intestinal myenteric plexus of burned rats].

OBJECTIVE: To elucidate the postburn change in the activity and the distribution of nitric oxide synthase (NOS) in rat intestinal myenteric plexus. METHODS: The activity and distribution of NOS were quantitatively and locationally studied by histochemical staining with NADPH-diaphorase (NDP), a marker for NOS, and whole mount preparation technique. RESULTS: NOS was widely distributed in whole intestine wall, especially in myenteric plexus. The majority of NOS positive neurons displayed either round or oval shape. There were some varicosities string of bead-like structure in the nerve fibers and which were accompanied by blood vessels and muscular fibers. There was no significant postburn change in the density of NOS positive neurons in myenteric plexus (P < 0.05). Nevertheless the NOS activity of neurons decreased obviously (P < 0.05 similar 0.01). Meanwhile, it was found after injury that there were indistinction of the structure of NOS positive neuron, more breaking of nerve fibers, leading to the lack of integral web of nerve fibers and obvious decrease of NOS positive varicosities in nerve fibers. CONCLUSION: After burn injury, the NOS positive neural structure in myenteric plexus of rat small intestine was damaged with the decrease in NOS activity. Simultaneously, there was impairment of the releasing route of nitric oxide (NO). All these changes might be closely related to intestinal structural damage and dysfunction after burn injury.

Animals↗

PubMed2003

Aging of the myenteric plexus: neuronal loss is specific to cholinergic neurons.

Neuron loss occurs in the myenteric plexus of the aged rat. The myenteric plexus is composed of two mutually exclusive neuronal subpopulations expressing, respectively, nitrergic and cholinergic phenotypes. The goal of the present study, therefore, was to determine if neuron loss is specific to one phenotype, or occurs in both. Ad libitum fed virgin male Fischer 344 rats of 3 and 24 months of age were used in each of two neuronal staining protocols (n=10/age/neuron stain). The stomach, duodenum, jejunum, ileum, colon, and rectum were prepared as whole mounts and processed with either NADPHd or Cuprolinic Blue to stain, respectively, the nitrergic subpopulation or the entire population of myenteric neurons. Neuron numbers and sizes were determined for each preparation. Neuron counts from 24-month-old rats were corrected for changes in tissue area resulting from growth. There was no age-related loss of NADPHd-positive neurons for any of the regions sampled, whereas significant losses of Cuprolinic Blue-labeled neurons occurred in the small and large intestines of 24-month-old rats. At the two ages, the average neuron sizes were similar in the stomach and small intestine for both stains, but neurons in the large intestine were significantly larger at 24 months. In addition, numerous swollen NADPHd-positive axons were found in the large intestine at 24 months. These findings support the hypothesis that age-related cell loss in the small and large intestines occurs exclusively in the cholinergic subpopulation. It appears, however, from the somatic hypertrophy and the presence of swollen axons that the nitrergic neurons are not completely spared from the effects of age.

Aging↗

PubMed1982

An ultrastructural study of neurons and non-neuronal cells in the myenteric plexus of the rabbit colon.

The myenteric plexus of the rabbit colon showed a degree of structural organization that was unusually high for the peripheral nervous system, providing a basis for the complex integrative activity which is known to occur. It resembled central nervous tissue in several respects: a wide range of neuron types was present; the proportion of glial cells to neurons was about 2:1; and there was a densely packed, avascular neuropil, not penetrated by connective tissue. Most neurons had at least one surface exposed to the extraganglionic space. Clear evidence was obtained for spontaneous neuronal degeneration. Three types of non-neuronal (glial) cells were observed: Type 1, which was most common, contained many 10 nm 'gliofilaments' and resembled enteric glial cells or astrocytes in the central nervous system; Type 2, composing about 5% of the glial cells, had few filaments; Type 3 was seen only rarely, had a small dark nucleus, little cytoplasm, may have been of extraganglionic origin and resembled microglia of the central nervous system. Fibroblast-like cells were also present in extraganglionic sites. Schwann cells could not be identified within the myenteric ganglia.

Animals↗

PubMed1992

Opioid-controlled adenylate cyclase in the guinea-pig myenteric plexus is confined to nerve somata.

Previous studies with the electrically stimulated longitudinal muscle-myenteric plexus preparation of the guinea-pig ileum suggested that opioid control of adenylate cyclase is confined to nerve somata. No indication was found for an opioid effect on the enzyme at nerve terminals of the neuro-muscular junction. The aim of the present investigation was to directly study the effect of opioids on cAMP generation in nerve fragments associated with somata or terminals of the myenteric plexus. Employing the ultracentrifugation technique an enrichment of cell organelles in fractions relating to either somata or terminals was achieved. Opioid binding studies revealed specific mu-receptors which in both fractions were regulated by GTP. Challenge of these fractions with forskolin and prostaglandin E1, respectively, resulted in an increased production of cAMP regardless of their neuroanatomical assignment. Examining the response of neuronal material to the selective mu-opioid DAMGO ([D-Ala2, MePhe4, Gly-ol5]enkephalin) revealed an inhibitory action on cAMP synthesis in somata-enriched fractions. No effect of DAMGO was observed in material linked to nerve terminals, although the presence of mu-opioid receptors and adenylate cyclase has been demonstrated. We conclude that opioid control of adenylate cyclase in the myenteric plexus of the guinea pig is confined to nerve somata.

Adenylyl Cyclases↗

PubMed1976

Serotonin accumulation in the guinea-pig myenteric plexus: ion dependence, structure-activity relationship and the effect of drugs.

The specific accumulation of serotonin in neurons of the guinea-pig myenteric plexus was examined. Nonadrenergic neurons have been shown to be responsible for this accumulation. Serotonin accumulation, known to be sodium-dependent, was found to be inhibited by elevating the external potassium concentration. Accumulation was inversely related to the concentration of potassium and was also decreased in the presence of 0 mM Ca++ or 12 mM Ca++. The affinity of analogous molecules for the myenteric plexus was greatly reduced in compounds which had no alkyl amino side chain, in which the amino group was methylated or which had no 5-hydroxyl group. Most analogs competitively inhibited serotonin accumulation and 6-hydroxytryptamine was demonstrated by histofluorescence to be taken up into the myenteric plexus after chemical sympathectomy with 6-hydroxydopamine. Serotonin accumulation was also inhibited by tricyclic antidepressants and amphetamines. The inhibition of serotonin accumulation by these compounds differed from their inhibition of accumulation of norepinephrine. As in the central nervous system, chlorimipramine was the most potent tricyclic antidepressant against accumulation of serotonin while desmethylimipramine was the most potent inhibitor of the accumulation of norepinephrine. Amphetamines were more effective inhibitors of serotonin accumulation than were tricyclic antidepressants, but all of these drugs were more effective against the accumulation of norepinephrine than serotonin. This study confirms the existence of a unique population of axons int he mammalian myenteric plexus which are distinguishable by their characteristic accumulation of serotonin and have not been found elsewhere in the peripheral nervous system.

Amphetamines↗

PubMed2002

Cholinergic and nitrergic interneurones in the myenteric plexus of the human colon.

BACKGROUND: Myenteric interneurones are involved in the reflexes that control the motility of the human colon. AIMS: The distribution of choline acetyltransferase (ChAT) and nitric oxide synthase (NOS) immunoreactivity in myenteric interneurones was investigated in this study. METHODS: DiI (1,1'- didodecyl 3,3,3',3'-indocarbocyanine perchlorate) was applied to the myenteric plexus of the human colon followed by organotypic culture. Retrogradely labelled neurones, with projections longer than motor neurones (>10 mm), were studied to exclude motor neurone populations. ChAT and NOS immunoreactivity was then determined in the interneurones. RESULTS: We found that 90% of interneurones projecting orally contained ChAT and none contained NOS. Ninety five per cent of descending interneurones were labelled with ChAT and/or NOS antisera; 46% contained NOS immunoreactivity alone, 20% contained ChAT immunoreactivity alone, and 29% contained both ChAT and NOS. Anally directed interneurones had significantly longer projections than orally projecting interneurones. CONCLUSIONS: Nearly all interneurones contain either NOS or ChAT immunoreactivity. Orally projecting interneurones are of two types: 90% contain ChAT alone and the remainder contain immunoreactivity for neither ChAT nor NOS. There are three main types of anally projecting interneurones: the largest, which contains NOS but not ChAT, and the two smaller classes which contain ChAT and NOS, and CHAT alone.

Aged↗

PubMed1976

Loperamide binding to opiate receptor sites of brain and myenteric plexus.

Loperamide, a new antidiarrheal agent, was tested to determine whether its biological activity involves binding to opiate receptor sites. Loperamide and morphine competitively inhibited 3H-naloxone binding to homogenates a guinea-pig brain and myenteric plexus. The Kp values obtain in the presence of Na+ were: morphine, 9.60-10(-9) M (brain), 1.66-10(-7) M (myenteric plexus); loperamide, 7.20-10(-9) M (brain), 1.33-10(-7) M (myenteric plexus); naloxone, 4.78-10(-10) M (brain), 1.27-10(-9) M (myenteric plexus. In the absence of Na+, binding a loperamide and morphine to brain homogenate was enhanced while the binding of naloxone was reduced. Morphine (IC50 = 7.5-10(-8) M) and loperamide (IC50 = 6.9-10(-9) M) inhibited the electrically induced contractions of longitudinal muscle from guinea-pig ileum, and naloxone competitively antagonized these effects. The Kd value calculated for the interaction of naloxone with binding sites associated with the contracting muscle was between 0.98-10(-9) M and 1.85-10(-9) M. In the mouse hot plate test, subcutaneous administration of morphine (minimal effective dose = 6.6 mugmol/kg) and loperamide (minimal effective dose = 78 mugmol/kg) delayed the response to heat stimuli and this effect was completely blocked by prior administration of naloxone. In the anesthetixed dog, intravenous administration of morphine (100 mug/kg) and loperamide (100 mug/kg) enhanced the contractile activity of circular muscle in proximal and distal duodenum, distal ileum and proximal colon but duodenal longitudinal muscle was relaxed; these effects were completely reversed by subsequent administration of naloxone. It is concluded that loperamide binds to opiate receptor sites and possesses opiate agonist activity both in vivo and in vitro.

Analgesics, Opioid↗

PubMed2000

Marked morphological differences in the myenteric plexus between the mesenteric and antimesenteric sides of small bowel in premature infants.

BACKGROUND: The gastrointestinal tract appears morphologically prepared for oral feeding by the end of the second trimester, but many of the physiological processes required for efficient enteral nutrition are not developed fully until 33 to 34 weeks' gestation. Myenteric plexus is well recognized as an important regulator of peristaltic activity. Whole-mount preparation technique produces a 3-dimensional picture to better show the neuronal networks branching and interconnections. The aim of this study was to investigate neurone density and morphology of the myenteric plexus in premature infants using whole-mount technique. METHODS: Full-thickness small and large bowel specimens were collected at autopsy from 6 premature babies (gestational age, 26 to 32 weeks) who died without evidence of gastrointestinal disease. Whole-mount preparation of the myenteric plexus was made and stained with NADPH-diaphorase and Acetylcholinesterase (AChE) histochemistry. The stained myenteric network was measured with a computer image analysis system. Controls included 4 full-term babies who died of nongastrointestinal disease. RESULTS: In premature infants there were striking differences in neuronal density of myenteric plexus in the mesenteric and antimesenteric border of small bowel. The differences in neuronal density in mesenteric and antimesenteric border of small bowel gradually became less striking as the gestation progressed with no differences evident at gestational age 32 weeks. CONCLUSIONS: This study shows for the first time that the neurone density of myenteric plexus is significantly higher in the mesenteric border of the small bowel compared with antimesenteric border in premature infants. The marked morphological differences observed in neurone density in the small bowel of premature infants may contribute to immature small bowel activity.

Autopsy↗

PubMed1985

5-hydroxytryptamine releases adenosine 5'-triphosphate from nerve varicosities isolated from the myenteric plexus of guinea-pig ileum.

5-Hydroxytryptamine (5-HT)-evoked release of ATP from nerve varicosities isolated from the myenteric plexus of guinea pig ileum was investigated. 5-HT released ATP from myenteric varicosities by a Ca2+-dependent mechanism. The EC50 for release of ATP was 7 X 10(-7) M 5-HT. 5-HT-evoked release of ATP was not blocked by tetrodotoxin (TTX), indicating that release was not initiated by the opening of Na+-channels in the isolated myenteric varicosities. Release of ATP by 5-HT was diminished to 56% of control values by in vivo pretreatment of the guinea-pig with 6-hydroxydopamine (6-OHDA, 250 mg kg-1, i.p.) for 24 h. 6-OHDA pretreatment caused extensive destruction of noradrenergic varicosities as indicated by an 87% loss of noradrenaline content. Quipazine (5 X 10(-6) M) and methysergide (10(-4) M) caused a small release of ATP and blocked subsequent 5-HT-induced release of ATP. Metergoline (2.5 X 10(-5) M), (+)-tubocurarine (7 X 10(-5) M) and cocaine (10(-4) M) decreased 5-HT-induced ATP release. 5-Methoxytryptamine (10(-4) M), picrotoxin (3.5 X 10(-6) M), spiroperidol (10(-6) M), morphine (1.3 X 10(-6) M) and phenoxybenzamine (3.7 X 10(-7) M) were ineffective. The results demonstrate a 5-HT-receptor-mediated release of ATP from noradrenergic and possibly non-adrenergic varicosities in the myenteric plexus of guinea-pig ileum. The 5-HT-induced release of ATP is consistent with a possible transmitter, cotransmitter or modulatory role for ATP in the myenteric plexus.

Adenosine Triphosphate↗

PubMed2001

Distribution of nitric oxide synthase in stomach myenteric plexus of rats.

AIM: To study the distribution of nitric oxide synthase (NOS) in rat stomach myenteric plexus. METHODS: The distribution of NOS in gastric wall was studied in quantity and location by the NADPH-diaphorase (NDP) histochemical staining method and whole mount preparation technique. RESULTS: NOS was distributed in whole stomach wall, most of them were located in myenteric plexus, and distributed in submucosal plexus.The shape of NOS positive neurons was basically similar, most of them being round and oval in shape. But their density, size and staining intensity varied greatly in the different parts of stomach. The density was 62+/-38 cells mm(2) (antrum), 43+/-32 cells/mm(2) (body), and 32+/-28 cells mm(2) (fundus), respectively. The size and staining intensity of NOS positive neurons in the fundus were basically the same, the neurons being large and dark stained, while they were obviously different in antrum. In the body of the stomach, the NOS positive neurons were in an intermediate state from fundus to antrum. There were some beadlike structures which were strung together by NOS positive varicosities in nerve fibers, some were closely adherent to the outer walls of blood vessels. CONCLUSION: Nitric oxide might be involved in the modulation of motility, secretion and blood circulation of the stomach, and the significant difference of NOS positive neurons in different parts of stomach myenteric plexus may be related to the physiologic function of stomach.

Animals↗

PubMed1991

Regulation of G proteins by chronic opiate and clonidine treatment in the guinea pig myenteric plexus.

G proteins have been implicated in the development of opioid dependence of the guinea pig myenteric plexus as chronic fentanyl elevates G0/i alpha and pertussis toxin prevents this phenomenon. Therefore, the present study investigates G proteins more closely in this peripheral nerve plexus after chronic exposure to addictive drugs of the opiate and nonopiate type. After 6 days of treatment with either the mu receptor ligand fentanyl, the kappa- agonist U-50,488H or the alpha-2 adrenergic receptor ligand clonidine, at doses which render the myenteric plexus tolerant and dependent, the G protein subunits Go alpha and G beta were quantified by immunoblot analysis by using polyclonal antisera. Regardless of the drug used, these G proteins were found to be significantly increased in particulate membrane preparations linked to nerve somata and nerve terminals. This increase in G protein subunits is developed maximally after 6 days, is dose-dependent and reversible upon termination of the drug supply. The concentrations found elevated return to control levels within 4 to 5 days after commencing withdrawal. The common increase of Go alpha and G beta subunits observed after chronic opiate or clonidine exposure is associated with the phenomenon of cross-dependence among all drugs studied. The findings may suggest that in the guinea pig myenteric plexus multiple inhibitory receptor types make use of a common pool of G proteins.

Adrenergic alpha-Agonists↗

PubMed1990

Morphological changes of the myenteric plexus neurons in the bullfrog (Rana catesbeiana) duodenum during metamorphosis.

Myenteric plexus neurons of the duodenum in the bullfrog Rana catesbeiana were examined during metamorphosis by the Gros-Bielschowsky silver impregnation method and electron microscopy. Larval type neurons with slender and curved cell soma were recognized in the duodenum of the premetamorphic tadpole. They degenerate and decrease in number during early metamorphic climax through shrinkage of the cell soma and autolysis of the cytoplasm. These larval type neurons reduce to debris and then disappear. Two new cell types (adult type neurons) subsequently appear. These new neurons develop and increase in number during late climax and after metamorphosis. Those that appear first are large type A neurons each with a prominent axon and they stain darkly with silver. They enlarge during late stages. Subsequently small type B neurons appear which stain weakly with silver. They increase the number of their dendrites, change their shape, but enlarge only slightly during late development. In summary, therefore, it is concluded that during metamorphosis, the larval myenteric plexus neurons in the bullfrog duodenum are replaced by two new populations of adult neurons.

Animals↗

PubMed1984

Characterization of the stimulus-induced release of immunoreactive substance P from the myenteric plexus of the guinea-pig small intestine.

The release of immunoreactive substance P (I-SP) from the myenteric plexus of the isolated guinea-pig small intestine and some of its characteristics have been investigated. Depolarizing stimuli, i.e. elevation of the extracellular K+ concentration or electrical field stimulation, increased the release of I-SP, the extent of the increase being dependent on the strength of the stimulus. Omission of Ca2+ from the bath medium prevented the stimulus-induced release of I-SP. Tetrodotoxin inhibited only the increase in I-SP release brought about by electrical stimulation but not that caused by elevated K+ concentrations. Gel exclusion chromatography on Sephadex G-25 showed that all the I-SP released by depolarization was co-eluted with authentic substance P. The methionine enkephalin analogue FK 33-824 significantly reduced the stimulus-induced release of I-SP, an effect that was prevented by the opiate antagonist naloxone. Naloxone alone significantly enhanced the stimulus-induced release of I-SP, which suggests that endogenously released opioid peptides also exert an inhibitory action on myenteric substance P-containing neurons. Putative excitatory neurotransmitters of the myenteric plexus, such as acetylcholine, bombesin, cholecystokinin octapeptide, and neurotensin, stimulated the release of I-SP in a tetrodotoxin-sensitive manner, whereas 5-hydroxytryptamine seemed ineffective. Capsaicin, known to release substance P from sensory neurons, also failed to alter the release of I-SP. The finding of a Ca2+-dependent release of I-SP caused by depolarizing stimuli further supports the concept that substance P is a neurotransmitter within the myenteric plexus. The activity of myenteric substance P-containing neurons appears to be controlled by a number of other putative enteric neurotransmitters.

Animals↗

PubMed1998

Inhibitory effects of nitric oxide donors on nitric oxide synthesis in rat gastric myenteric plexus.

We investigated whether nitric oxide (NO) exerts an inhibition on its own synthesis in the gastric myenteric plexus in rats. Nonadrenergic, noncholinergic relaxations in response to transmural electrical stimulation (TS) were markedly antagonized by NG-nitro-L-arginine methyl ester, (10(-4) M) and abolished by tetrodotoxin (10(-6) M). Pretreatment with various NO donors (3-morpholino-sydnonymide [SIN-1 (3 x 10(-7) to 3 x 10(-6) M)], S-nitroso-N-acetylpenicillamine (10(-6) to 10(-5) M), sodium nitroprusside (10(-8) to 3 x 10(-8) M) and 8-bromoquanosine 3', 5'-cyclic monophosphate [8-bromo-cGMP (10(-6) to 3 x 10(-6) M)]) significantly inhibited TS-evoked nonadrenergic, noncholinergic relaxations in a dose-dependent manner. In contrast, vasoactive intestinal polypeptide (10(-8) M)-induced relaxations were not affected by SIN-1 or 8-bromo-cGMP. TS evoked a significant increase in 3H-citrulline formation, which was completely abolished by calcium-free medium, NG-nitro-L-arginine methyl ester, (10(-4) M) and tetrodotoxin (10(-6) M). 3H-citrulline formation evoked by TS was significantly inhibited by SIN-1 (10(-7) to 10(-5) M) and 8-bromo-cGMP (10(-7) to 10(-5) M) in a dose-dependent manner. The inhibitory effect of SIN-1 was partially prevented by 1H-[1,2, 4]oxadiazolo[3,4-a]quinoxalin-1-one (10(-5) M), a guanylate cyclase inhibitor. We conclude that NO synthesis in the gastric myenteric plexus is negatively regulated by NO and cGMP. This suggests an autoregulatory feedback mechanism of NO synthesis in the gastric myenteric plexus.

Animals↗

PubMed1986

Pharmacological characterization of rat jejunal contractility after chronic ablation of the myenteric plexus.

The authors have pharmacologically characterized longitudinal muscle contractility of the isolated rat jejunum chronically devoid of myenteric neurons. The myenteric plexus of a 3- to 4-cm segment of rat jejunum was ablated by serosal application of the cationic surfactant benzalkonium chloride (BAC). Fifteen days after treatment, both BAC-treated and untreated control jejunal segments were removed from each animal for pharmacological studies. BAC-treated tissues did not respond to the ganglionic stimulants nicotine, 1,1-dimethyl-4-phenylpiperazinium iodide and McN-A-343 or to the acetylcholinesterase inhibitor physostigmine. Short-pulse duration transmural electrical stimulation (0.1 msec) caused a frequency-dependent, tetrodotoxin-sensitive contraction in control but not BAC-treated tissues. Long-pulse duration transmural electrical stimulation (5.0 msec) contracted both control and BAC-treated jejunum. These contractions were partially reduced but not completely blocked by tetrodotoxin. To assess smooth muscle function, the mechanical responses to the muscarinic receptor agonist carbachol were examined. Carbachol contracted both control and BAC-treated tissues with maximal responses and ED50 values that were not significantly different. In addition, the maximal tension development produced by 10(-2) M barium chloride in similar lengths of control and BAC-treated jejunal segments was not significantly different. These studies demonstrate that chronic ablation of the myenteric plexus by serosal application of BAC essentially eliminates neuronally mediated responses without a concomitant alteration in longitudinal muscle contractility. Because nerve-mediated longitudinal muscle responses are lost despite the presence of an intact submucosal plexus in the BAC-treated jejunum, our data suggest that the motor neurons innervating the rat jejunal longitudinal muscle are located in the myenteric plexus.

(4-(m-Chlorophenylcarbamoyloxy)-2-butynyl)trimethy↗

PubMed1999

c-Fos expression in the myenteric plexus, spinal cord and brainstem following injection of formalin in the rat colonic wall.

Fos expression induced by injection of dilute formalin (50 microl, 5% in physiological saline) into the colonic wall was examined in the myenteric plexus, lumbosacral spinal cord and brainstem of the rat. The aims of this study were (i) to determine whether neurons in these regions express Fos in response to the injection of formalin into the colon and (ii) to examine whether administration of an alpha 2 adrenoceptor agonist modulates Fos expression. Tissues were removed 2 h after the injection of saline or formalin. Saline injected in the colon induced Fos in enteric glia in the myenteric plexus. The number of Fos immunoreactive nuclei significantly increased in both myenteric neurons and enteric glia after the injection of formalin. Similarly, Fos immunoreactive neuronal nuclei were significantly increased in the spinal cord, area postrema and nucleus of the solitary tract after the injection of formalin. Pretreatment of rats with the alpha 2 adrenoceptor agonist xylazine (2, 4 and 8 mg/kg) 15 min before the injection of formalin, dose-dependently reduced the number of Fos immunoreactive neuronal and glial nuclei in the myenteric plexus, and neuronal nuclei in the spinal cord and brainstem. Simultaneous administration of xylazine (8 mg/kg) and the alpha 2 adrenoceptor antagonist yohimbine (1 mg/kg) reversed the effects of xylazine in the spinal cord and brainstem, but not in the myenteric plexus. These data show that injection of formalin in the colonic wall results in Fos expression in myenteric neurons and enteric glia, and neurons in the spinal cord and brainstem. This may be due to the direct chemical stimulation of the innervation of the colon and/or the subsequent acute colitis. The observed neuronal Fos expression can be modulated by an alpha 2 adrenoceptor agonist through noradrenergic pathways and/or reduction of the excitability of the enteric neural circuitry.

Adrenergic alpha-Agonists↗

PubMed2003

Induction of neuronal nitric oxide synthase by sympathetic denervation is mediated via alpha 2-adrenoceptors in the jejunal myenteric plexus.

Nitric oxide (NO) is an important nonadrenergic, non-cholinergic (NANC) inhibitory neurotransmitter in the gastrointestinal tract. In previous studies, neuronal nitric oxide synthase (nNOS) in the jejunal myenteric plexus, a key enzyme responsible for the release of NO, has been demonstrated to increase after splanchinic ganglionectomy (sympathetic nerve transection). The alpha2-adrenoceptor is known to be one of the most important receptors which controls intestinal motility. In the present study, we examined the effect of application of the alpha2-adrenoceptor agonist, clonidine hydrochloride, on nNOS expression in the rat jejunal myenteric plexus after splanchinic ganglionectomy. Clonidine (0.1-1 mg/kg, i.p.) or saline was administered for 5 days after the splanchinic ganglionectomy. The nNOS expression and nNOS mRNA were detected by immunohistochemistry and in situ hybridization for nNOS mRNA, respectively. In the rats treated with vehicle after the splanchinic ganglionectomy, nNOS expression in the myenteric plexus significantly increased compared with sham-operated rats. The increases in nNOS protein and mRNA after splanchinic ganglionectomy were significantly reversed by clonidine treatment. Clonidine-treated naive rats showed no difference in nNOS expression compared with sham-operated rats. These data suggest that nNOS expression in the jejunal myenteric plexus after splanchinic ganglionectomy is regulated by the alpha2-adrenoceptor and that the alpha2-adrenoceptor may play an important role in abnormal intestinal motility following splanchinic ganglionectomy in rat jejunum.

Animals↗