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PubMed1996

Effect of muscle denervation on the expression of substance P in the ventral raphe-spinal pathway of the rat.

The medullary raphe nuclei, wherein serotonin (5-HT) coexists with substance P (SP) and thyrotropin-releasing hormone (TRH), innervate lower motor neurons in the spinal cord ventral horn by means of the ventral raphe-spinal pathway. Destruction of the ventral raphe-spinal pathway is associated with deficient recovery of denervated muscle, indicating that it may exert a trophic effect upon lower motor neurons. To determine whether SP could be a trophic factor for lower motor neurons within the ventral raphe-spinal pathway, the effect of muscle denervation with botulinum toxin type A on SP-encoding beta-preprotachykinin mRNA in the rat medullary raphe was examined by in situ hybridization histochemistry. Silver grain density over hybridized medullary raphe neurons was increased by up to 11%, although the number of hybridized neurons did not change in denervated as compared to control rats. Increased SP gene expression in the medullary raphe in response to motor unit lesioning suggests that raphe-spinal SP may be trophic to lower motor neurons.

Animals↗
PubMed1993

Neovascularisation precedes neural changes in the rat groin skin flap following denervation: an immunohistochemical study.

We have employed immunohistochemical techniques to study neural and vascular changes in rat skin flaps. Following partial or total denervation, flaps were studied at 4, 7 or 12 days using antisera to PGP 9.5 (panneural marker), the neuropeptides CGRP (sensory nerves) and CPON (adrenergic nerves) and an endothelial marker VWF. In partially denervated flaps, moderate increases in PGP-immunoreactive (PGP-IR) and CGRP-IR nerves and a mild increase in CPON-IR nerves in immediate surrounding skin preceded smaller increases in similar nerves around the pedicle. Following total denervation, mild increases in all nerve types at these locations were accompanied by a marked increase of these nerves in distant surrounding skin, 1-2 cm from the suture line. A gradual increase in endothelial cell staining (VWF) of blood vessels was seen in surrounding skin, flap beds and pedicles. Angiogenesis preceded flap reinnervation which occurred initially from surrounding skin, and later from the base, with sensory fibres appearing first.

Animals↗
PubMed1988

Embryonic and neonatal myosin heavy chain in denervated and paralyzed rat skeletal muscle.

Using immunofluorescence procedures with specific polyclonal and monoclonal antimyosin antibodies we have found that embryonic and neonatal myosin heavy chains (MHCs), which in rat skeletal muscle disappear during the first weeks after birth, are reexpressed in adult muscle after denervation. Reactivity for embryonic and neonatal MHCs was detected in some fibers as early as 3 days after denervation, became more evident by 7 days, and occurred exclusively in the type 2A fiber population. Paralysis of innervated muscles by tetrodotoxin block of the sciatic nerve also resulted in the reappearance of embryonic and neonatal MHCs in type 2A fibers. Significant variation in the degree of immunoreactivity was observed in different segments of the same muscle fiber, suggesting that coordination of muscle fiber nuclei in the control of myosin heavy chain gene expression is partially lost following denervation.

Aging↗
PubMed1990

Regulation of muscle sodium channel transcripts during development and in response to denervation.

We have recently described the cloning and functional expression of a new sodium channel subtype, microI, isolated from a denervated rat skeletal muscle cDNA library. In studies described here, we have used RNase protection and Northern blot analyses to examine the expression of microI mRNA in different tissues and in neonatal, adult, and adult denervated muscle. We found that microI transcripts were not expressed in brain or heart, or in the myogenic cell line L6, even after differentiation to myotubes. Transcripts for microI were present at low levels in neonatal skeletal muscle and increased to maximum levels in adult tissue, paralleling the expression of tetrodotoxin (TTX)-sensitive sodium currents. Surprisingly, denervation of adult muscle was also followed by a rise in microI mRNA, at a time when TTX-insensitive currents reappear. These results show that expression of this channel subtype is regulated by tissue type, development, and innervation.

Animals↗
PubMed1983

Effects of chronic sino-aortic denervation in male rats on regional catecholamine levels and turnover and on neuroendocrine function.

A four week sino-aortic denervation produces an increase of adrenaline (A) turnover in the anterior but not the posterior hypothalamus and a selective reduction of dopamine stores in the anterior hypothalamus. Furthermore, the mean arterial blood pressure and heart rate are unchanged in conscious animals, and a selective increase in LH secretion is observed. The activation of a compensatory vasodepressor adrenergic mechanism in the anterior hypothalamus may in part be responsible for the maintenance of a normal mean arterial blood pressure after chronic sino-aortic denervation. The neurochemical changes in the hypothalamic area may also be related to the increase in LH secretion found after chronic sino-aortic denervation.

Animals↗
PubMed1989

Enhanced acetylcholine release from denervated atria: intrinsic neural supersensitivity.

Atrial tissue from denervated dog hearts was incubated with [3H]choline. When compared with controls, nicotine released more acetylcholine (ACh) from denervated atria at 10(-5) and 2 x 10(-5) M, but not at 5 x 10(-5) M. In parallel contractility studies using tissue from these same atria, the negative inotropic response to nicotine was enhanced at 5 x 10(-6) and 10(-5) M, but not at 2 x 10(-5) or 5 x 10(-5) M nicotine. These results indicate that denervation (i.e. decentralization) supersensitivity of the intrinsic cardiac nerves of canine hearts is characterized by enhanced release of ACh.

Acetylcholine↗
PubMed1994

Decreased density of binding sites for the Ca2+ channel antagonist [3H]isradipine after denervation of rat vas deferens.

Radioligand binding assays were performed with the selective antagonist of dihydropyridine-sensitive Ca2+ channels [3H]PN200-110 (isradipine) in rat vas deferens, before and 7 days after denervation, and data were compared with those obtained for K(+)-induced contractions, which are Ca(2+)-dependent. The density (Bmax) of dihydropyridine binding sites was decreased to almost one-third of its normal value after denervation. The respective affinity (KD) was not significantly changed. In addition, it was observed that the K(+)-induced tonic contraction, which corresponded to 55 +/- 2% of the respective phasic contraction, was decreased to 41 +/- 3% after denervation. It is assumed that the decreased density of Ca2+ channels causes a decrease in K(+)-induced influx of Ca2+ and consequently of the corresponding tonic contraction. These results indicate that autonomic innervation can regulate the density of dihydropyridine-sensitive Ca2+ channels in the rat vas deferens.

Animals↗
PubMed1983

Rapid decline in acetylcholine release and content of rat extensor digitorum longus muscle after denervation.

The amount of acetylcholine (ACh) and choline (Ch) in normal and denervated rat extensor digitorum longus (EDL) muscles, as well as that released spontaneously from these muscles, was determined by an extremely sensitive gas chromatographic-mass spectrometric assay method. We found decreases in ACh content and spontaneous, resting ACh release as early as 8 h after denervation. The ACh content decreased to a plateau of 30% of control by 11 h; ACh release attained a plateau of 50% of control several hours later. These results showed that in denervated EDL muscles ACh content and spontaneous release (measured biochemically) decreased before nerve-evoked and spontaneous quantal release (measured physiologically) ceased at most synapses. The rapid reduction in ACh, or possibly in other substances that may be released with ACh, may be an important factor in initiating postsynaptic degenerative changes after nerve transection. Choline content and choline resting release increased significantly at both 1 and 3 days after nerve transection. These increases may be related to onset of postsynaptic neuromuscular degenerative changes.

Acetylcholine↗
PubMed1983

Reinnervation is followed by necrosis in previously denervated skeletal muscles of dystrophic hamsters.

Hind leg muscles of dystrophic hamsters were continually denervated by multiple crushes of the sciatic nerve to as long as 93 days of age. In these muscles, the prevalence of centronucleated fibers which is a cumulative index of prior necrosis, remained very low. In control dystrophic muscles the prevalence of centronucleated fibers increased steadily to approximately 80% where it leveled off. By omitting further crushes in other groups of animals, previously denervated muscles became adequately reinnervated. In the reinnervated muscles the prevalence of centronucleated fibers steadily increased throughout the necrotic phase of dystrophy at a rate that was comparable to corresponding stages of the natural history of the disease. These experiments indicated that continued denervation was effective in negating skeletal muscle fiber necrosis throughout the necrotic phase and that the electromechanical activity of muscle fibers which allows muscle fiber necrosis was not a time-locked factor.

Animals↗
PubMed1985

Partial purification from mammalian peripheral nerve of a trophic factor that ameliorates atrophy of denervated muscle.

Atrophy in a denervated muscle results from the disuse caused by paralysis of the muscle, and from the loss of special nerve-derived trophic substances. Crude preparations of protein from rat or sheep sciatic nerves have been shown to prevent the nondisuse atrophy of the rat's extensor digitorum longus muscle when injected into the denervated muscle daily for 1 week. Aqueous extracts of sheep sciatic nerves were fractionated by gel-liquid chromatography. After each step of purification, the trophic activities of the various fractions were assayed in the rat. Cross-sectional areas of type IIB muscle fibers in the denervated extensor digitorum longus were measured to determine which injected fraction contained the active principle. Affinity chromatography on concanavalin A-agarose revealed that the trophic substance was a glycoprotein. Further fractionation by gel filtration indicated that the active substance had a molecular weight in the range of 90,000 to 130,000. Ion-exchange chromatography on DEAE-cellulose yielded an active fraction containing substances with isoelectric points between 7.0 and 7.2, determined by polyacrylamide gel isoelectric focusing. This active fraction was resolved into 15 bands on sodium dodecyl sulfate-gel electrophoresis. Two bands had apparent molecular weights of 91,300 and 127,400. The active factor was shown thus to be a glycoprotein, molecular weight approximately 100,000, isoelectric point approximately 7.0. It may be one of two protein bands that are similar to it in molecular weight.

Animals↗
PubMed1986

Effect of denervation during development upon membrane potential and intracellular potassium and sodium activities of skeletal muscle of the rat.

Potassium and sodium ion-selective microelectrodes were used in vitro to investigate the effect of denervation of fast-twitch skeletal muscle (extensor digitorum longus) at 5 days of age upon subsequent development of the resting membrane potential. Normally, during the first 3 weeks of life the balance of intracellular potassium and sodium changed to elevate potassium and to lower sodium. These changes were reflected in the development of a more hyperpolarized resting membrane. Periods of denervation delayed, or prevented, the changes in ion activities and membrane hyperpolarization from occurring. The results are compared with those found after denervation of adult skeletal muscle.

Animals↗
PubMed1986

Membrane potential and intracellular potassium and sodium activities after denervation of soleus muscles of neonatal rats.

Potassium and sodium ion-selective microelectrodes were used in vitro to investigate the depolarization of slow-twitch skeletal muscle fibers (soleus) following denervation at 5 to 6 days of age. The normal increase in intracellular potassium ion activity and decrease in sodium ion activity which occurs during the first 3 weeks of life were delayed or prevented by denervation. The results are compared with those found after similar periods of denervation of neonatal rat fast-twitch muscle.

Animals↗
PubMed1990

Protein synthesis is required for the denervation-triggered activation of acetylcholine receptor genes.

The effect of cycloheximide (CHX) on denervation-induced acetylcholine receptor (AChR) expression was investigated in chickens one day after nerve section, using probe excess solution hybridization to quantitate AChR alpha-subunit gene transcript levels and run-on analysis to measure subunit gene activity. The increase in alpha-subunit transcripts that normally follows denervation was prevented when drug treatment was commenced 2 h before or after denervation but was not blocked when CHX administration was begun 6 h after the operation. Drug-induced reduction of transcript levels results from decreased activity of genes coding for the alpha-, delta-, and gamma-subunits; in contrast, the transcription rates of several non-receptor genes are not affected by CHX. The results suggest that the de novo synthesis of a transcriptional activator is required as a mediating event in the signalling pathway linking the plasma membrane and AChR gene expression.

Animals↗
PubMed1991

Colonic motility in innervated and extrinsically denervated loops in dogs.

The control mechanism of canine colonic motor activity measured by means of chronically implanted force transducers was studied by comparing diurnal changes and migrating patterns in control dogs and dogs with innervated and extrinsically denervated colonic loops. Five force transducers (C1-C5) were placed on the colon, and the middle colon was transected to construct a loop including C2 and C3 transducers. Colonic continuity was established by an end-to-end anastomosis. In the fasted state, colonic motor complexes of 8-13 minutes' duration were observed to occur at intervals of 22-32 minutes in all three groups, but response to feeding was clearly different; significant enhancement of the colonic motor indexes lasting for 8-16 hours after feeding, which was observed at all recording sites in control dogs, was identified only in the proximal and distal colon in dogs with innervated and extrinsically denervated loops. In the innervated loop, significant enhancement of the motor indexes was observed only in the first 2 hours after feeding. In the extrinsically denervated loop, feeding did not induce any response. In both groups with loops, greater than 40% of the motor complexes that occurred in the proximal colon migrated to the distal colon directly across the anastomosis and less than 20% propagated to the loop. In addition, the migration time between the proximal and the distal colon was greatly reduced in both groups with loops compared with that in the control group. Another change observed within the loop was an increase in numbers of retrograde migrating colonic motor complexes. It is concluded that colonic motor activity is under the predominant control of intraluminal contents in the digestive state but that extrinsic nerves may play an important role in the response observed in the innervated loop in the first 2 hours after feeding, which should be defined as the gastrocolonic response in dogs. In the interdigestive state, the intrinsic nervous system and/or humoral factors may control the occurrence of colonic motor complexes.

Animals↗
PubMed1994

Normal fasting volume and postprandial emptying of the denervated donor gallbladder in liver transplant recipients.

BACKGROUND/AIMS: Truncal vagotomy causes gallbladder dilatation and possibly cholelithiasis. During liver transplantation, when the gallbladder is transplanted with the donor liver, the gallbladder and liver are extrinsically denervated. The aim of this study was to determine whether extrinsic denervation affects gallbladder volume and postprandial emptying. METHODS: To evaluate fasting gallbladder volume, 26 transplant recipients underwent ultrasonography. Twenty-eight normal volunteers were controls. To evaluate postprandial contractility, seven transplant recipients underwent radionuclide gallbladder-emptying studies. Gastric emptying and cholecystokinin release were simultaneously determined after a fatty meal to exclude a difference in gallbladder stimulus. Sixteen normal volunteers were controls. RESULTS: There were no differences in fasting gallbladder volume or postprandial contractility, gastric emptying, and cholecystokinin release between transplant patients and controls. Median fasting and postprandial gallbladder volumes for the transplant recipients (95% confidence) were 16 mL (12-34 mL) and 3 mL (0-8 mL), respectively, and for controls were 18 mL (13-21 mL; P = 0.73) and 3 mL (1-6 mL; P = 0.97), respectively. CONCLUSIONS: These data do not show gallbladder dilatation or impaired postprandial gallbladder contraction in the extrinsically denervated gallbladder. This finding suggests that gallbladder dilatation may be caused by the unopposed activity of the sympathetic system after truncal vagotomy.

Adult↗
PubMed1984

Effects of extrinsic denervation on net water transport and motility of the feline gallbladder in vivo.

The influence on the concentrating ability of the gallbladder after extrinsic denervation was studied in anesthetized cats, previously subjected to truncal vagotomy, and/or celiacectomy , and compared with sham-operated controls. Net water absorption was studied by perfusion techniques. Acute experiments were performed under basal conditions and alpha-adrenoceptor stimulation (iv infusion of norepinephrine (NE), 1 micrograms/kg X min). Gallbladder biopsies were studied by fluorescence microscopy to visualize and quantitate catecholamines. Three weeks after celiacectomy basal absorption had decreased significantly. In the short-term vagotomy group no changes were demonstrated. However, in the long-term vagotomy group there was a fourfold increase in absorptive capacity, which decreased to control levels after alpha-adrenoceptor blockade (phentolamine 1 mg/kg iv). Long-term vagotomy with subsequent celiacectomy caused no significant changes. Infusion of NE increased net water absorption by 70 +/- 16% in all experimental groups except in long-term vagotomized animals, where the high basal absorption was not further augmented. One hour after NE infusion controls returned to basal absorption rate, while denervated cats remained at stimulated levels. In long-term vagotomized gallbladders there were morphological signs of adrenergic proliferation (increased total number of nerve terminals, sprouting, and elevated levels of intraneuronal NE). In conclusion these results suggest that the adrenergic nervous system is important for full absorptive capacity of the gallbladder. The increased absorption after long-term vagotomy, abolished after alpha-adrenoceptor blockade, might well be explained by the parallel adrenergic proliferation. This hypothesis was further corroborated in animals with long-term vagotomy, where subsequent surgical adrenergic denervation restored basal absorption to control levels.(ABSTRACT TRUNCATED AT 250 WORDS)

Absorption↗
PubMed1975

Appearance of acetylcholinesterase and creatine kinase in plasma of normal chickens after denervation.

Evidence that acetylcholinesterase (AChE) activity is released from normal chick embryonic muscle fibers and from muscles of chickens with inherited muscular dystrophy suggested that denervated chick muscles, which have AChE properties similar to dystrophic muscles, would also release AChE. Bilateral denervation of the breast and wing muscles of normal chickens was followed by the appearance of AChE activity, distinguished from plasma cholinesterase by differential substrate hydrolysis, inhibitor sensitivity, and electrophoretic migration. Plasma creatine kinase (CK) activity was also elevated after denervation.

Acetylcholinesterase↗
PubMedDate not supplied

Increased T3 deiodination in dystrophic and neonatally denervated mouse muscle.

T3, free iodide levels and morphological features were compared in normal, 129 ReJ dy/dy dystrophic and neonatally denervated skeletal muscles of mice, killed 6 hr after a single intraperitoneal injection of iodine-labelled hormone. Both the dystrophic andthe denervated muscles were found to contain equal amounts of T3 but more iodide than the normal specimens. Increased iodide levels are considered to reflect augmented T3-catabolism by muscle dehalogenase and may indicate low free hormone levels in the soluble enzyme fraction of the cell, despite its normal overall T3 content. The close light-microscopic resemblance of 129 ReJ dy/dy dystrophy and neonatal denervation is confirmed. The possibility is discussed that one or several of the muscular dystrophies are forms of target organ hypothyroidism.

Animals↗