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PubMed1988

Sodium channel distribution in normal and denervated rodent and snake skeletal muscle.

1. Sodium channel current density was measured using the loose-patch voltage clamp technique. Innervated rat, mouse and snake muscle had the highest density of Na+ channels in the end-plate region. These high Na+ channel densities were maintained in denervated muscle. 2. Perijunctional membrane had a Na+ current density 5- to 10-fold greater than the density several hundred micrometres from the end-plate. In all muscles this concentration of channels near the end-plate persisted following denervation. 3. At the tendon Na+ current density fell to low values (approximately 1 mA/cm2). The decrease in density began about 300-500 microns from the tendon. This pattern was found in all snake twitch fibres and fast-twitch (EDL) rat and mouse muscle fibres. This reduction in channel density near the tendon was not affected by denervation. 4. Sodium channels in all regions of innervated rat and snake muscle fibres were highly sensitive to tetrodotoxin (TTX). Sodium channels in snake muscle remained sensitive to TTX after denervation. Sodium channels that are relatively resistant to TTX appeared in rat muscle after denervation. TTX-resistant channels were even more concentrated near the end-plate than were TTX-sensitive channels in innervated muscle. At the tendon TTX-resistant Na+ channel density decreased. 5. We conclude that although the nerve presumably directs the localization of Na+ channels during development, the ability to maintain this distribution and to control the distribution of newly appearing channels persists long after the nerve has been removed.

Action Potentials↗
PubMed1990

Substance P mediates neurogenic vasodilatation in extrinsically denervated guinea-pig submucosal arterioles.

1. Arteriolar diameter was measured using an optical method in preparations of guinea-pig submucosal plexus in vitro. Electrical stimulation of one or more neurones in ganglia of the submucosal plexus causes a cholinergic vasodilatation in normal animals. The vasomotor innervation to the arterioles was studied in guinea-pigs in which the extrinsic nerves to the intestine had been removed. Tissues were processed for immunohistochemistry after the in vitro experiments. 2. Extrinsic denervation resulted in complete loss of catecholamine fluorescence, NPY (neuropeptide Y) and CGRP (calcitonin gene-related peptide) immunofluorescence around the blood vessels and no neurogenic vasoconstriction was observed up to 60 days post-denervation. Vasodilatation in response to ganglionic stimulation was increased; smaller arterioles (outside diameter less than 40 microns) showed a greater enhancement of neurogenic vasodilatation than larger arterioles. 3. Nerve-evoked vasodilatations were only partially inhibited by muscarinic antagonists at 30-60 days after extrinsic denervations. 4. The non-cholinergic neurogenic vasodilatation was abolished by the substance P antagonists, spantide, [D-Arg1, D-Pro2, D-Trp7.9, Leu11]substance P and [D-Arg1, D-Phe5, D-Trp7.9, Leu11]substance P. These antagonists did not alter the cholinergic vasodilatation in normal or extrinsically denervated arterioles. 5. Exogenous substance P dilated all submucosal arterioles; the concentration which produced half-maximal vasodilatations was 2.5 mM in both normal and extrinsically denervated arterioles. Substance P antagonists inhibited the vasodilatation caused by substance P at concentrations similar to those needed to block nerve-mediated vasodilatation. 6. There was a strong correlation between the finding of non-cholinergic vasodilatation in response to ganglionic stimulation, and the presence of substance P-immunoreactive fibres running from ganglion to arteriole. This correlation did not exist for VIP (vasoactive intestinal peptide). 7. These results suggest that intrinsic intestinal substance P-containing nerve fibres supply submucosal arterioles after sympathetic efferents and sensory afferents are removed. Stimulation of these nerves releases substance P to produce arteriolar dilatation.

Animals↗
PubMed1991

Morphology of long-term denervated rat soleus muscle and the effect of chronic electrical stimulation.

1. Rat soleus muscles were denervated for 6-10 months; some of these were chronically stimulated for the last 3-8 weeks before recording. The muscles were fixed at physiological lengths and embedded in epoxy resin. 2. Sections for light microscopy were stained with p-phenylenediamine. Denervation reduced the mean cross-sectional area of fibres to 3% of controls (peak at 20 microns2). The cross-sectional areas of the stimulated fibres had a peak at 70 microns 2. In light micrographs of denervated muscles, the total number of fibres appeared to be reduced; however not all fibres could be identified (see paragraph (3)). 3. In the electron microscope, many fibres showed disarrayed myofilaments. Few fibres had more or less normal cross-striations. Muscle fibres as small as 1 micron in diameter were seen. The smallest fibres did not contain myofilaments. Some unequivocally necrotic fibres were seen. 4. Most stimulated denervated fibres showed an almost normal sarcomere pattern. Scattered throughout the muscle were single fibres as small as 2 microns in diameter, but these were well organized and could be recognized in the light microscope. Few fibres were necrotic. Often fibres were serially arranged. Satellite cells were prominent. 5. It is concluded that in long-term denervated rat soleus the original fibres are lost and those seen are the result of repeated cycles of regeneration and necrosis. Stimulation maintains the sarcomeres and probably prevents secondary degeneration and necrosis.

Actin Cytoskeleton↗
PubMed2002

Mouse muscle denervation increases expression of an alpha7 nicotinic receptor with unusual pharmacology.

Neuronal nicotinic alpha7 subunits have been found in chick and rat skeletal muscle during development and denervation. In the present study, reverse transcriptase-polymerase chain reaction was used to detect alpha7 subunit mRNA in denervated mouse muscle. To determine whether the alpha7 subunit forms functional nicotinic acetylcholine receptors (nAChRs) in muscle, choline was used to induce a membrane depolarization because choline has been considered a specific agonist of alpha7-containing (alpha7*) nAChRs. We found, however, that choline (3-10 mM) also weakly activates muscle nAChRs. After inhibiting muscle nAChRs with a specific muscle nAChR inhibitor, alpha-conotoxin GI (alphaCTxGI), choline was used to activate the alpha7* nAChRs on muscle selectively. Four weeks after denervation, rapid application of choline (10 mM) elicited a substantial depolarization in the presence of alphaCTxGI (0.1 microM). This component of the depolarization was never present in denervated muscles obtained from mutant mice lacking the alpha7 subunit (i.e. alpha7-null mice). The depolarization component that is resistant to alphaCTxGI was antagonized by pancuronium (3-10 microM) and by a 4-oxystilbene derivative (F3, 0.1-0.5 microM) at concentrations considered highly specific for alpha7* nAChRs. Another selective alpha7 antagonist, methyllycaconitine (0.05-5 microM), did not strongly inhibit this choline-induced depolarization. Furthermore, the choline-sensitive nAChRs showed little desensitization over 10 s of application with choline (10-30 mM). These results indicate that functional alpha7* nAChRs are significantly present on denervated muscle, and that these receptors display unusual functional and pharmacological characteristics.

Animals↗
PubMed1997

Influence of carotid denervation on the body-core temperature and metabolic responses to changes in ambient temperature during normoxemia and acute hypoxemia in guinea pigs during postnatal maturation.

Acute hypoxemia produces a decrease in body-core temperature (Tbc) in guinea pigs during postnatal maturation, although the factors mediating the response remain unknown. Experiments were therefore carried out to test the hypothesis that the carotid chemoreceptors and (or) baroreceptors mediate the decrease in Tbc during acute hypoxemia. Twelve guinea pigs, six carotid intact and six carotid denervated, were studied in a metabolic chamber to determine the influence of carotid denervation on the Tbc and metabolic (i.e., oxygen consumption) responses to changes in ambient temperature during normoxemia and during acute hypoxemia at 2, 3, and 4 weeks of age. Carotid denervation accentuated the decrease in Tbc in response to a decrease in ambient temperature during normoxemia at 2 and 3 weeks of age but not at 4 weeks of age without altering the metabolic response. This suggests that carotid denervation disrupted heat conservation mechanisms rather than heat production mechanisms in an age-specific manner. Furthermore, carotid denervation accentuated the decrease in Tbc and oxygen consumption in response to acute hypoxemia at all ages studied. This provides evidence that the carotid chemoreceptors and (or) baroreceptors do not mediate the decrease in Tbc that occurs in response to acute hypoxemia in guinea pigs during postnatal maturation.

Animals↗
PubMed1987

Supersensitivity to norepinephrine in chronically denervated kidneys: evidence for a postsynaptic effect.

Denervation supersensitivity in chronically denervated kidneys increases renal responsiveness to increased plasma levels of norepinephrine. To determine whether this effect is caused by presynaptic (i.e., loss of uptake) or postsynaptic changes, we studied the effect of continuous infusion of norepinephrine (330 ng/min, i.v.) and methoxamine (4 micrograms/min, i.v.), an alpha 1-adrenergic agonist that is not taken up by nerve terminals, on renal function of innervated and denervated kidneys. Ganglionic blockade was used to eliminate reflex adjustments in the innervated kidney and mean arterial pressure was maintained at preganglionic blockade levels by an infusion of arginine vasopressin. With renal perfusion pressure controlled there was a significantly greater decrease in renal blood flow (-67 +/- 9 vs. -33 +/- 8%), glomerular filtration rate (-60 +/- 9 vs. -7 +/- 20%), urine flow (-61 +/- 7 vs. -24 +/- 11%), sodium excretion (-51 +/- 15 vs. -32 +/- 21%), and fractional excretion of sodium (-50 +/- 9 vs. -25 +/- 15%) from the denervated kidneys compared with the innervated kidneys during the infusion of norepinephrine. During the infusion of methoxamine there was a significantly greater decrease from the denervated compared with the innervated kidneys in renal blood flow (-54 +/- 10 vs. -30 +/- 14%), glomerular filtration rate (-51 +/- 11 vs. -19 +/- 17%), urine flow (-55 +/- 10 vs. -39 +/- 10%), sodium excretion (-70 +/- 9 vs. -59 +/- 11%), and fractional excretion of sodium (-53 +/- 10 vs. -41 +/- 10%).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1991

Effect of renal denervation on plasma renin activity after aortic baroreceptor deafferentation.

Renal nerves are thought to play an important role in cardiovascular regulation under both normotensive and hypertensive conditions. In the present study the effect of renal denervation on the changes in plasma renin activity (PRA) after aortic baroreceptor deafferentation (tADN) were investigated in the rat. Bilateral renal denervation did not alter arterial pressure (AP, 100 +/- 4 mmHg; 1 mmHg = 133.32 Pa), heart rate (HR, 363 +/- 12 bpm), or PRA (2.9 +/- 0.6 ng.mL-1.h-1) compared with the respective sham renal denervation values of 106 +/- 3 mmHg (AP), 385 +/- 13 bpm (HR), and 3.3 +/- 0.7 ng.mL-1.h-1 (PRA). On the other hand, bilateral tADN resulted in significant increases in AP, HR, and PRA. One and 3 days after tADN, AP was 130 +/- 4 and 127 +/- 6 mmHg, HR was 461 +/- 15 and 463 +/- 20 bpm, and PRA was 9.1 +/- 3.0 and 11.9 +/- 4.5 ng.mL-1.h-1, respectively. Renal denervation before tADN prevented the increases in AP and PRA, but it did not affect the increase in HR. These data indicate that renal denervation does not alter basal PRA in normotensive animals but prevents the increased renin release observed in neurogenic hypertension. These data suggest that the increased PRA may be one of several factors that contributes to the elevated AP after tADN.

Animals↗
PubMed2005

Osteoactivin upregulates expression of MMP-3 and MMP-9 in fibroblasts infiltrated into denervated skeletal muscle in mice.

In this study, we examined pathophysiological roles of osteoactivin, a functionally unknown type I membrane glycoprotein, in mouse skeletal muscle atrophied by denervation (sciatic neurectomy). Denervation increased the amounts of osteoactivin, vimentin, matrix metalloproteinase-3 (MMP-3), and MMP-9 in mouse gastrocnemius muscle. Interestingly, immunohistochemical analysis revealed that vimentin, MMP-3, and MMP-9 were mainly present in fibroblast-like cells infiltrated into denervated mouse gastrocnemius muscle, whereas osteoactivin was expressed in the sarcolemma of myofibers adjacent to the fibroblast-like cells. On the basis of these findings, we reasoned that osteoactivin in myocytes was involved in activation of the infiltrated fibroblasts. To address this issue, we examined effects of osteoactivin on expression of MMPs in fibroblasts in vitro and in vivo. Overexpression of osteoactivin in NIH-3T3 fibroblasts induced expression of MMP-3, but not in mouse C(2)C(12) myoblasts, indicating that osteoactivin might functionally target fibroblasts. Treatment with recombinant mouse osteoactivin increased the amounts of collagen type I, MMP-3, and MMP-9 in mouse NIH-3T3 fibroblasts. The upregulated expression of these fibroblast marker proteins was significantly inhibited by heparin, but not by an integrin inhibitor, indicating that a heparin-binding motif in the extracellular domain might be an active site of osteoactivin. In osteoactivin-transgenic mice, denervation further enhanced expression of MMP-3 and MMP-9 in fibroblasts infiltrated into gastrocnemius muscle, compared with wild-type mice. Our present results suggest that osteoactivin might function as an activator for fibroblasts infiltrated into denervated skeletal muscles and play an important role in regulating degeneration/regeneration of extracellular matrix.

Animals↗
PubMed1989

Terminal cisternae of denervated rabbit skeletal muscle: alterations of functional properties of Ca2+ release channels.

Terminal cisternae (TC) of skeletal muscle represent the specialized compartment from which Ca2+ is released into the myoplasm after a propagated action potential. In this study we have investigated the morphology, protein composition, and Ca2+ release properties of TC isolated from rabbit gastrocnemius muscle 2 wk after nerve sectioning. Thin-section electron microscopy showed that TC vesicles from denervated muscle were enriched in calsequestrin (CS) and contained a larger fraction of the junctional sarcoplasmic reticulum (SR), as judged by membrane profiles with morphologically intact feet structures. Accordingly, the yield of junctional SR from denervated muscle was twice that of control muscle, and the protein pattern of TC vesicles exhibited an increase in junctional protein components, e.g., CS and the 350-kDa protein. The larger content of the 350-kDa protein, or ryanodine receptor (F.A. Lai, H. Erickson, E. Rousseau, Q.-Y. Liu, and G. Meissner, Nature Lond. 331: 315-319, 1988; T. Imagawa, J. S. Smith, R. Coronado, and K. P. Campbell. J. Biol. Chem. 262: 10636-10643, 1987; L. Hymel, M. Inui, S. Fleischer, and H. Schindler, Proc. Natl. Acad. Sci. USA 85:441-445, 1988) was paralleled by an increased binding site density (Bmax) for ryanodine binding in denervated muscle TC. The effects of ruthenium red, a Ca2+ release blocker, on Ca2+ loading rate and Ca2+-ATPase activity suggested that TC from denervated muscle were less permeable to Ca2+. After active Ca2+ loading, both doxorubicin and caffeine induced Ca2+ release from isolated TC, yet Ca2+ release rates were reduced in denervated muscle TC.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine Triphosphate↗
PubMed1994

Sarcoplasmic reticulum Ca2+ pump expression in denervated skeletal muscle.

This study was undertaken as one approach to better understand how contractile activity regulates excitation-contraction coupling phenotype in skeletal muscle. The effects of denervation on the expression of the sarcoplasmic reticulum (SR) Ca(2+)-adenosinetriphosphatase (ATPase), a key protein of the contraction-relaxation cycle, was analyzed in fast-twitch (FT) and slow-twitch (ST) skeletal muscle. Muscle mass, mRNA, and protein expression of specific isoforms of the sarco(endo)plasmic reticulum Ca(2+)-ATPase (SERCA) and contractile parameters related to muscle relaxation were measured in rat soleus and extensor digitorum longus (EDL) muscles at 1, 4, 7, 14, and 28 days after sciatic nerve transection. Wet muscle mass decreased to 35% of control by 28 days of denervation in both soleus and EDL muscles (P < 0.05). Northern and Western analyses showed decreases in mRNA and protein expression of the slow Ca2+ pump isoform (SERCA2a) in the denervated soleus muscle and in the fast Ca2+ pump isoform (SERCA1) in the denervated EDL muscle, particularly at later time points. There was no change in the expression of the alternate isoform in either muscle type. Prolongation of twitch contraction times, slowed rates of tension development, and leftward shifts in frequency-tension curves were consistent with the reduced Ca2+ pump density and suggested slowed Ca2+ handling in SR or denervated ST and FT muscles. The results are in marked contrast with those previously reported in non-weight-bearing muscle induced by biomechanical unloading.

Animals↗
PubMed2001

Calpain 3 mRNA expression in mice after denervation and during muscle regeneration.

Lack of functional calpain 3 in humans is a cause of limb girdle muscular dystrophy, but the function(s) of calpain 3 remain(s) unknown. Special muscle conditions in which calpain 3 is downregulated could yield valuable clues to the understanding of its function(s). We monitored calpain 3 mRNA amounts by quantitative RT-PCR and compared them with those of alpha-skeletal actin mRNA in mouse leg muscles for different types of denervation and muscle injury. Intact muscle denervation reduced calpain 3 mRNA expression by a factor of 5 to 10, while alpha-skeletal actin mRNA was reduced in a slower and less extensive manner. Muscle injury (denervation-devascularization), which leads to muscle degeneration and regeneration, induced a 20-fold decrease in the mRNA level of both calpain 3 and alpha-skeletal actin. Furthermore, whereas in normal muscle and intact denervated muscle, the full-length transcript is the major calpain 3 mRNA, in injured muscle, isoforms lacking exon 6 are predominant during the early regeneration process. These data suggest that muscle condition determines the specific calpain 3 isoform pattern of expression and that calpain 3 expression is downregulated by denervation.

Actins↗
PubMed2004

AMP kinase is not required for the GLUT4 response to exercise and denervation in skeletal muscle.

An acute bout of exercise increases muscle GLUT4 mRNA in mice, and denervation decreases GLUT4 mRNA. AMP-activated protein kinase (AMPK) activity in skeletal muscle is also increased by exercise, and GLUT4 mRNA is increased in mouse skeletal muscle after treatment with AMPK activator 5-aminoimidazole-4-carboxamide-1-beta-D-ribofuranoside(AICAR). These findings suggest that AMPK activation might be responsible for the increase in GLUT4 mRNA expression in response to exercise. To investigate the role of AMPK in GLUT4 regulation in response to exercise and denervation, transgenic mice with a mutated AMPK alpha-subunit (dominant negative; AMPK-DN) were studied. GLUT4 did not increase in AMPK-DN mice that were treated with AICAR, demonstrating that muscle AMPK is inactive. Exercise (two 3-h bouts of treadmill running separated by 1 h of rest) increased GLUT4 mRNA in both wild-type and AMPK-DN mice. Likewise, denervation decreased GLUT4 mRNA in both wild-type and AMPK-DN mice. GLUT4 mRNA was also increased by AICAR treatment in both the innervated and denervated muscles. These data demonstrate that AMPK is not required for the response of GLUT4 mRNA to exercise and denervation.

Aminoimidazole Carboxamide↗
PubMed1988

Phenylarsine oxide and denervation effects on hormone-stimulated glucose transport.

Insulin and insulin-like growth factor I (IGF-I) stimulate glucose transport in skeletal muscle through separate receptors. The proximal postreceptor events in coupling insulin and IGF-I receptors to glucose transport have been suggested to differ. Denervation of skeletal muscle produces a postreceptor insulin resistance presumably at an early step in the signaling cascade. We examined the effects of denervation and phenylarsine oxide (PAO), an agent believed to block insulin action on transport at a postreceptor step, on insulin and IGF-I stimulated 2-deoxy-D-glucose transport in isolated solei. Denervation (24 h) produced severe IGF-I resistance without affecting IGF-I receptor number or affinity. PAO inhibited insulin and IGF-I stimulation of transport in control muscles by approximately 90 and approximately 70%, respectively. In denervated muscle PAO inhibited transport stimulation by both hormones less than in controls. Conclusions are that 1) skeletal muscle insulin and IGF-I receptors signal transport mainly through a PAO-sensitive mechanism, but IGF-I's action involves a larger PAO-resistant component; 2) the denervation-induced postreceptor resistance of glucose transport to both hormones involves primarily the PAO-sensitive pathway.

Adenosine Triphosphate↗
PubMed1990

Free amino acids in muscle: effect of muscle fiber population and denervation.

One hindlimb of each rat was denervated by sectioning the sciatic nerve. Three days later, soleus, plantaris, and gastrocnemius muscles of the sham hindlimb and the contralateral denervated hindlimb were excised and analyzed for intracellular concentrations of 23 free amino acids and the dipeptides carnosine and anserine. Compared with the sham soleus (slow-twitch) muscle, the sham plantaris and gastrocnemius (fast-twitch) muscles showed 57-81% lower concentrations of histidine, glutamine, glutamate, aspartate, and serine and also 32-78% lower levels of taurine, citrulline, phosphoserine, and ornithine. On the other hand the fast-twitch muscles exhibited 31% higher concentrations of free glycine and alanine and 113-127% higher levels of carnosine and anserine than the soleus muscle. The denervation caused greater changes in soleus muscle than in the other two muscles. The denervation-induced changes in soleus muscle included 38-87% increases in concentrations of free valine, leucine, isoleucine, and glutamate associated with 21-56% decreases in the levels of glutamine, glycine, aspartate, serine, alanine, and citrulline. It is concluded that both muscle fiber population and muscle denervation have an independent effect on the intracellular concentrations of free amino acids in muscles.

Amino Acids↗
PubMed1999

Regulation of skeletal muscle UCP-2 and UCP-3 gene expression by exercise and denervation.

The factors that regulate gene expression of uncoupling proteins 2 and 3 (UCP-2 and UCP-3) in skeletal muscle are poorly understood, but both genes are clearly responsive to the metabolic state of the organism. Therefore, we tested the hypothesis that denervation and acute and/or chronic exercise (factors that profoundly affect metabolism) would alter UCP-2 and UCP-3 gene expression. For the denervation studies, the sciatic nerve of rat and mouse hindlimb was sectioned in one leg while the contralateral limb served as control. Northern blot analysis revealed that denervation was associated with a 331% increase (P < 0.001) in UCP-3 mRNA and a 200% increase (P < 0. 01) in UCP-2 mRNA levels in rat mixed gastrocnemius (MG) muscle. In contrast, denervation caused a 53% decrease (P < 0.001) in UCP-3 and a 63% increase (P < 0.01) in UCP-2 mRNA levels in mouse MG. After acute exercise (2-h treadmill running), rat UCP-3 mRNA levels were elevated (vs. sedentary control) 252% (P < 0.0001) in white gastrocnemius and 63% (P < 0.05) in red gastrocnemius muscles, whereas UCP-2 levels were unaffected. To a lesser extent, elevations in UCP-3 mRNA (22%; P < 0.01) and UCP-2 mRNA (55%; P < 0.01) levels were observed after acute exercise in the mouse MG. There were no changes in either UCP-2 or UCP-3 mRNA levels after chronic exercise (9 wk of wheel running). These results indicate that acute exercise and denervation regulate gene expression of skeletal muscle UCPs.

Animals↗
PubMed2000

Amelioration of denervation-induced atrophy by clenbuterol is associated with increased PKC-alpha activity.

Rat soleus muscle was denervated for 3 or 7 days, and total membrane protein kinase C (PKC) activity and translocation and immunocytochemical localization of PKC isoforms were examined. Dietary administration of clenbuterol concomitant with denervation ameliorated the atrophic response and was associated with increased membrane PKC activity at both 3 (140%) and 7 (190%) days. Of the five PKC isoforms (alpha, epsilon, theta, zeta, and mu) detected in soleus muscle by Western immunoblotting, clenbuterol treatment affected only the PKC-alpha and PKC-theta forms. PKC-alpha was translocated to the membrane fraction upon denervation, and the presence of clenbuterol increased membrane-bound PKC-alpha and active PKC-alpha as assayed by Ser(657) phosphorylation. PKC-theta protein was downregulated upon denervation, and treatment with clenbuterol further decreased both cytosolic and membrane levels. Immunolocalization of PKC-theta showed differences for regulatory and catalytic domains, with the latter showing fast-fiber type specificity. The results suggest potential roles of PKC-alpha and PKC-theta in the mechanism of action of clenbuterol in alleviating denervation-induced atrophy.

Adrenergic beta-Agonists↗
PubMed1987

Cholinergic mechanisms in the pancreas after extrinsic denervation in the rat.

Extrinsic denervations of the pancreas were carried out in rats using bilateral truncal abdominal vagotomy and/or celiac and superior mesenteric ganglionectomy. Chronic fistulas were produced and pancreatic secretion was then measured in conscious animals. In all three groups of extrinsically denervated animals the basal pancreatic secretion was significantly decreased by 15-44% (fluid), 32-59% (bicarbonate output), and 33-43% (protein output). Meal-stimulated secretion was decreased in denervated animals by 38-57% (fluid), 32-44% (bicarbonate output), and 36-64% (protein output). In extrinsically denervated rats, atropine inhibited basal pancreatic fluid by 26-38%, bicarbonate output by 46-71%, and protein output by 63-80%, whereas hexamethonium inhibited basal protein output by 36-58%. These data indicate that cholinergic mechanisms persist in the pancreas after extrinsic denervation. This may correspond either to the spontaneous activity of intrapancreatic excitatory cholinergic neurons or to the drive of these neurons by preganglionic fibers running through nonclassic (such as duodenopancreatic) pathways. No important difference was observed between the effects of vagotomy and those of celiac and superior mesenteric ganglionectomy, indicating that most of the excitatory vagal fibers for the exocrine pancreas run through the celiac pathway and that adrenergic fibers had little effect on the conditions tested.

Animals↗
PubMed1988

Effect of denervation on initiation and coordination of gastroduodenal motility in turkeys.

The effect of total extrinsic denervation of the stomach on the rhythmicity and coordination of the gastroduodenal cycle was determined in domestic turkeys. The vagus and two gastric branches of the sympathetic nerve were sectioned at the level of the glandular stomach. Motilities of the glandular stomach, proximal duodenum, and caudal thin muscle of the muscular stomach were monitored via implanted strain gauge transducers for 1 h every other day. Denervation had no significant effect on initiation of contractions or frequency of gastric contractions in fed birds, but fasted birds whose stomachs were extrinsically denervated exhibited significantly slower contractions than controls. In addition, denervation uncoupled the coordination of the duodenal and gastric contractions in the gastroduodenal cycle. Moreover, birds with extrinsically denervated stomachs exhibited a cephalic phase of gastric motility that was significantly delayed in onset compared with controls. These results suggest the existence of both a neural and endocrine component in the avian gastric response to the sight of food. Extrinsic input seems to be an important modulator of gastric motility in birds and is essential for the normal coordination of the gastroduodenal contraction cycle.

Animals↗