Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “DENERVATION”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 847 records · Page 47Linked to original sources
PubMed1989

Increase in the amount of adenylate cyclase in rat gastrocnemius muscle after denervation.

After section of the sciatic nerve, the basal adenylate cyclase (AC) activity in rat gastrocnemius muscle increased 6-7 times per membrane protein and about 2 times per whole muscle in the following 30 or 40 days. The AC activity in the muscle 30 days after denervation was increased about 4 times by forskolin. Calcitonin gene-related peptide (CGRP) also increased the adenylate cyclase activity in the denervated muscle. The binding of [3H]-forskolin (10nM) to cells isolated from gastrocnemius muscle was examined to determine the amount of AC molecules. Inhibition of [3H]-forskolin binding by increasing amounts of unlabeled forskolin gave a sigmoid curve with a IC50 value of 3 x 10(-7) M. Results showed that the number of [3H]-forskolin binding sites per cell was higher on the denervated side than on the control side, like the basal AC activity. The IC50 values for inhibition by unlabeled forskolin of binding of [3H]-forskolin were similar to muscles on the control and denervated sides. These results suggest that an increase in the AC activity induced by denervation was due to an increase in the numbers of AC molecules in the muscle.

Adenylyl Cyclases↗
PubMed1992

Cyclic adenosine monophosphate accumulation and beta-adrenergic binding in unweighted and denervated rat soleus muscle.

Unweighting, but not denervation, of muscle reportedly "spares" insulin receptors, increasing insulin sensitivity. Unweighting also increases beta-adrenergic responses of carbohydrate metabolism. These differential characteristics were studied further by comparing cyclic adenosine monophosphate (cAMP) accumulation and beta-adrenergic binding in normal and 3-day unweighted or denervated soleus muscle. Submaximal amounts of isoproterenol, a beta-agonist, increased cAMP accumulation in vitro and in vivo (by intramuscular [IM] injection) to a greater degree (P less than .05) in unweighted muscles. Forskolin or maximal isoproterenol had similar in vitro effects in all muscles, suggesting increased beta-adrenergic sensitivity following unweighting. Increased sensitivity was confirmed by a greater receptor density (Bmax) for [125I]iodo-(-)-pindolol in particulate preparations of unweighted (420.10(-18) mol/mg muscle) than of control or denervated muscles (285.10(-18) mol/mg muscle). The three dissociation constant (Kd) values were similar (20.3 to 25.8 pmol/L). Total binding capacity (11.4 fmol/muscle) did not change during 3 days of unweighting, but diminished by 30% with denervation. This result illustrates the "sparing" and loss of receptors, respectively, in these two atrophy models. In diabetic animals, IM injection of insulin diminished cAMP accumulation in the presence of theophylline in unweighted muscle (-66% +/- 2%) more than in controls (-42% +/- 6%, P less than .001). These results show that insulin affects cAMP formation in muscle, and support a greater in vivo insulin response following unweighting atrophy. These various data support a role for lysosomal proteolysis in denervation, but not in unweighting, atrophy.

Animals↗
PubMed1980

Unilateral mesolimbicocortical dopamine denervation decreases locomotion in the open field and after amphetamine.

Unilateral denervation of the mesolimbicocortical dopaminergic (DA) system was produced by microinjections of 6-hydroxydopamine (6-OHDA) into the right or left anterolateral hypothalamus after desmethylimipramine pretreatment. Unilateral DA denervation was confirmed by the marked loss of fluorescent fibers in mesolimbic DA terminal fields in brains processed for catecholamine histofluorescence with the glyoxylic acid-paraformaldehyde method. Such unilateral DA denervation significantly decreased the locomotor exploration of an open field and the locomotor response to d-amphetamine (1.5 mg/kg). These results demonstrate that unilateral mesolimbococortical DA denervation is sufficient, and that bilateral denervation of a single amphetamine or a decrease of locomotion in the open field. The results are consistent with the hypothesis that the mesolimbicocortical DA system energizes behavior, but does not direct it.

Amphetamine↗
PubMed1982

Denervated and intact kidney responses to norepinephrine infusion in conscious dogs.

Effects of moderately hypertensive norepinephrine (NE) infusion on the function of denervated and innervated kidney were determined in conscious dogs chronically prepared by surgical splitting of the urinary bladder performed to enable separate urine collection from each kidney. While blood pressure increased 23 +/- 4 mm Hg and renal hemodynamics tended to increase slightly, sodium excretion of the denervated but not innervated kidney decreased significantly. This indicated a NE-stimulated increase in tubular sodium reabsorption. The effect was limited to the denervated kidney, possibly due to hypersensitivity of this organ's tubules to the circulating catecholamine. Previous blockade of alpha-receptors (phentolamine) appeared to blunt the dissociated response of the two kidneys to NE, whereas beta-receptor blockade (propranolol) did not affect it. This suggests that increasing sodium reabsorption of the denervated kidney depended on stimulation of tubular alpha-receptors. NE infusion impaired urine concentration equally in the intact and denervated kidney.

Animals↗
PubMed1986

Neural regulation of adrenal chromaffin cell function in the mouse: fate and distribution of [3H]dopamine in denervated adrenal medulla.

The distribution and time course of appearance and decline of radioactivity in denervated adrenal medulla of mice injected with [3H]dopamine was examined by autoradiography. Radioactivity irradiated from [3H]dopamine was increased from 7.5 min to 30 min, then decreased rapidly in both adrenaline-storing (A) cells and noradrenaline-storing (NA) cells of either intact or denervated adrenals. In subcortical A cells, the incorporation of radioactivity was increased by denervation while in NA cells and in A cells in the center of the medulla, the increment was not significant. In the denervated adrenals, the decline of [3H]dopamine-derived radioactivity was slower than that in the intact gland. The denervation increased the gradient in radioactivity from the surface to the center of the medulla. The present results suggest that the sensitivity to neuronal suppression of dopamine uptake in subcortical A cells is different from that in A and NA cells in the rest of the gland. The results also indicate a functional heterogeneity within a single type of chromaffin cells.

Adrenal Medulla↗
PubMed1993

Proliferation of mast cells in the smooth muscle of denervated rat jejunum.

Mast cell hyperplasia and changes in phenotypic characteristics subsequent to myenteric and extrinsic denervation of a segment of rat jejunum were studied. The myenteric plexus and extrinsic nerves were ablated by serosal application of the cationic surfactant benzyldimethyltetradecylammonium chloride. There was a four-fold increase in the number of mast cells in the smooth muscle layers 15 days after denervation. This increase was sustained for at least 90 days after treatment. No increase in mast cell number was observed in the villus-crypt axis of the jejunum. Berberine sulfate fluorescent detection of heparin-containing mast cells demonstrated that a change in mast cell phenotype occurred between 20 and 90 days after the denervation procedure. The fact that myeloperoxidase activity was the same in denervated and control tissue within 5 days of denervation demonstrates the lack of a chronic inflammatory reaction. Our results suggest that mast cells might play a role in the gut wall re-modeling processes.

Animals↗
PubMed1986

Mechanical properties of denervated amphibian muscle.

Denervated amphibian muscle does not show the prolongation of action potential found in mammalian denervated muscle. It was, therefore, predicted that denervated amphibian muscle would not show prolongation of the mechanical twitch. The sartorius muscles in one leg of toads--Xenopus borealis--were denervated for 140-268 days. Isometric twitch time to peak, time to half relaxation and twitch/tetanus ratio were not changed following denervation, confirming our prediction. Twitch tension decreased to 68% and tetanic tension decreased to 75% of control values. The maximum velocity of unloaded shortening (muscle length/s) was also unchanged.

Action Potentials↗
PubMed1989

Activity-independent modulation of acetylcholine receptor levels in rat skeletal muscle following neonatal denervation.

Following denervation of adult muscle, levels of acetylcholine receptor (AChR) increase; normal, low levels are restored only after muscle reinnervation. After neonatal denervation, we found a large initial increase in AChR levels during the first days postsurgery, as in adult denervated muscle. However, 1 week after denervation, total AChR levels decreased in the absence of any sign of reinnervation. By 3 weeks after surgery, near-normal levels of AChR were restored and extrajunctional AChR had disappeared. Thus, in sharp contrast to adult muscle, in young denervated muscle a down-regulation of AChR occurs without recovery of innervation and normal muscle contractile activity. These results suggest that different mechanisms regulate the levels of AChR in developing and adult skeletal muscle.

Acetylcholinesterase↗
PubMed1985

Autotomy following limb denervation: effects of sparing selected afferents.

Lesions of the brachial plexus are often followed by inflammation, self-inflicted scratching and autotomy of the denervated extremity. If innervation of the shoulder girdle muscles was spared, this denervation syndrome was decreased in incidence and intensity as compared to a full brachial plexus section. Spared innervation increased the latency between the appearance of inflammation and autotomy, revealing a strong linkage between the site of inflammation and the site of autotomy attack. Plexus lesions, which spared one of the nerves of the distal limb, also decreased the incidence and intensity of autotomy and shifted self-attack from autotomy to scratching wounds. Subsequent section of this nerve produced a two-stage brachial plexus denervation, and the cumulated autotomy was markedly less than that produced by a single-stage brachial plexus denervation. Scratching wounds and autotomy exhibited similar latencies. Scratching was directed towards areas of partial innervation and autotomy towards areas of total denervation. The results are discussed in terms of the possible contributions of dysesthesia inflammation and ischemia in scratching behavior and autotomy.

Animals↗
PubMed1982

Cell proliferation in denervated muscle: time course, distribution and relation to disuse.

The effects of denervation on skeletal muscle fibers have been intensively investigated, but the effects on other cell types within muscle tissue are not well understood. In the present experiments, cell proliferation was analyzed in mouse extensor digitorum longus muscles denervated for periods of one day to six weeks. Incorporation of tritiated thymidine into DNA increased 36 h after denervation, reached a maximum at a level twenty times control at 4 days, and returned towards control values by 7 days. Incorporation first increased in the endplate area, but 12 h later involved the entire muscle. Six weeks after denervation, muscles labeled at 4 days had lost 90% of the total label. Muscle disuse, produced by tetrodotoxin block of the nerve for up to 4 days, did not result in a proliferative response. Thus, cell proliferation after denervation is not a response to simple disuse, but rather to a nerve- or muscle-related mitogen. Since the response is mostly distributed throughout the entire muscle, the mitogen probably emanates from muscle fibers.

Animals↗
PubMed1982

The potentiating action of acetylcholine on the chemosensitivity of denervated skeletal muscle.

The acetylcholine sensitivity of soleus and extensor digitorum longus muscles of young rats was studied in vitro by measuring the isometric tension and membrane depolarisation developed in response to bath application of acetylcholine. Contractures of denervated muscles to acetylcholine gradually increased when the same concentration of acetylcholine was applied at 10 min intervals up to 60 min incubation whilst contractures evoked by potassium sulphate did not change significantly. The twitch tension of the muscles elicited in response to direct electrical stimulation did not increase and direct electrical stimulation failed to increase the acetylcholine sensitivity. Increased responses in vitro to acetylcholine were observed only in muscles denervated between 2 and 10 days previously with an optimum increase in sensitivity at 4-6 days. The increases in sensitivity were due to an action of acetylcholine since muscles left untreated exhibited no increases. Responses to carbamylcholine chloride, which is not hydrolysed by acetylcholinesterase, also increased. Membrane depolarisations in response to acetylcholine increased in a similar manner to the contracture responses in both soleus and extensor digitorum longus muscles, whilst the resting membrane potentials did not change. Denervated muscles which had been treated with acetylcholine bound more 125I-labelled alpha-bungarotoxin than muscles which had not been treated with acetylcholine. Denervated soleus muscles which had been previously blocked with unlabelled alpha-bungarotoxin responded to applications of acetylcholine with a gradually increasing depolarisation response and subsequently bound more [125I]alpha-bungarotoxin than muscles left without acetylcholine treatment. The possibility is discussed that acetylcholine acts upon the surface membranes of denervated muscles to increase the number of active acetylcholine receptors.

Acetylcholine↗
PubMed1982

Source of the stimulus for nerve terminal sprouting in partially denervated muscle.

The topological positions of nerve terminal sprouts in partially denervated rat sternocostal muscles were analysed. Sprouted nerve terminals were found only within 200 microns of a denervated muscle fibre, but were not necessarily within 200 microns of a denervated endplate. From this it was concluded that the sprout-inducing factor released from denervated muscle fibres does not necessarily arise from the denervated endplate, but may be released along the length of the muscle fibre. It is proposed that sprout factor is released during the incorporation of acetylcholine receptors into the muscle fibre membrane.

Animals↗
PubMed1984

Endplate topography of denervated and disused rat neuromuscular junctions: comparison by scanning and light microscopy.

The effect of denervation and tetrodotoxin-induced muscle disuse on endplate structure was investigated in rat hind-limb muscles. The endplate was visualized by light microscopic cholinesterase staining and by scanning electron microscopy. Denervation resulted in a reduction in histochemically determined endplate dimensions proportionate to the decrease in muscle fiber circumference. Scanning electron microscopy, on the other hand, revealed a flattening or more often collapse of primary grooves with a reduction in the width of the endplate but no longitudinal shrinkage. Primary groove area per se was not measurable due to the loss of primary groove structural integrity. Thus, the apparent histochemical diminution of endplate length after denervation was artefactual, probably due to loss of cholinesterase activity and impeded access of substrate. In disuse, cholinesterase staining revealed a similar reduction in endplate girth with fiber atrophy but with a corresponding increase in endplate length. Scanning electron microscopy of disused muscle fibers confirmed these histochemical findings and the overall preservation of primary groove area. Disuse also resulted in an increase in the number of intrasynaptic primary groove branches as visualized by scanning electron microscopy. Finally, a specialized endplate "raised area", prominent in soleus muscle, was greatly reduced after disuse but much less so after denervation. Thus, after denervation, primary groove structural integrity is lost and the shape of the endplate passively follows that dictated by circumferential loss of surface membrane. In disused muscle, presence of an intact axon preserves the structure and area but not the orientation of the primary grooves which are distorted by fiber atrophy. Disuse also strongly affects other endplate surface structures visualized by scanning electron microscopy.

Animals↗
PubMed1991

Morphological, neurochemical, and behavioral studies on serotonergic denervation and graft-induced reinnervation of the rat hippocampus.

A procedure was developed to conduct simultaneously immunocytochemical and neurochemical studies on the serotonergic system in adjacent 300-micron-thick slices of rat hippocampus. This procedure was applied to correlate morphological (innervation pattern and density), neurochemical (5-hydroxytryptamine and 5-hydroxyindolacetic acid levels and [3H]5-hydroxytryptamine uptake and release) and behavioral (spatial learning) effects of neurotoxin-induced denervation and reinnervation by grafting fetal mesencephalic raphe cells. Intracerebroventricular injections of a low dose of 5,7-dihydroxytryptamine caused a discrete serotonergic denervation of the hippocampus. Eleven months after lesioning, 5-hydroxytryptamine and 5-hydroxyindolacetic acid levels and [3H]5-hydroxytryptamine uptake capacity were decreased by 50-60%. By this time, the residual fibers displayed an enhanced vulnerability towards K(+)-induced depolarization. Grafting of a fetal raphe cell suspension resulted in a reinnervation of the host hippocampus. The pattern of reinnervation was comparable to control innervation and the density was supranormal at the level of the graft. As observed semiquantitatively, the innervation density decreased with distance from the core of the graft. Neurochemical studies showed that the fibers were capable of synthesizing, metabolizing and releasing 5-hydroxytryptamine. The turnover of 5-hydroxytryptamine in both the denervated and the reinnervated hippocampus was comparable to that in control tissue. Previous behavioral testing of the denervated and of the denervated and implanted animals did not reveal any effect on spatial learning, either in an individual or in a social test paradigm. The latter data substantiate the notion that interference with the hippocampal serotonergic innervation does not hamper adequate spatial learning.

5,7-Dihydroxytryptamine↗
PubMed1986

Liquid sucrose and fructose intake in male and female liver denervated rats.

Male and female rats were liver denervated [hepatic vagal branch transection (VAG-B), hepatic artery-portal vein denervations (H-ART) or total liver denervation (TOTAL)] and sham operated (SHAM). Rats were given chow along with exposure to sucrose and fructose solutions. Chow intakes and body weight gains of all experimental groups were similar to their SHAMS, but the male H-ART group weighed more than the male VAG-B group. Denervated male and female rats consumed amounts of 30% sucrose solution similar to their SHAMS; however, the female H-ART group took more than the female TOTAL rats. Female VAG-B and male H-ART groups drank more of a 30% fructose solution than their other groups. Mean 15% fructose intakes, for both sexes, of denervated rats were similar to their SHAMS. The data are not supportive for a role of liver satiety afferents in fructose and sucrose intake but do raise the possibility that autonomic nervous system balance to the liver could influence the rats' ingestion of these sugars. If true, the mechanism(s) must be generally subtle and somewhat sex variable.

Animals↗
PubMed1993

Recovery potential of muscle after partial denervation: a comparison between rats and humans.

The response to partial denervation is compared for the tibialis anterior muscle in the rat and the thenar muscle group in the human. Partial denervation in the human was a result of spinal cord injury, while partial denervation in the rat was induced by sectioning of the L4 ventral root. In some animals, a spinal cord transection at the T12-13 level was also performed to determine whether spinal cord injury affected the sprouting capability of motoneurons caudal to the injury site. Motor units were isolated by intramuscular microstimulation in the human and by ventral root splitting in a terminal experiment in the rat. Motor unit numbers were estimated by dividing the amplitude of the electromyogram (EMG) and the peak twitch force in response to maximum stimulation of the muscle nerve by the average unit EMG and twitch force, respectively. In both the rat and the human, surviving motor units enlarged as a function of the degree of partial denervation. Moreover, all surviving motor units appeared to enlarge proportionately. The limit to sprouting was tested systematically in the rat. On average, single motor units enlarged up to about five times their original size, resulting in the ability to compensate for up to 80% of motoneuron loss. The reason for this limit remains unclear, but histological data suggest that sprouting may be confined to the more distal regions of the motor axon, such that reinnervation of denervated muscle fibers is confined to the territory of the original motor unit.

Animals↗
PubMed1985

Influence of denervation on the cholinergic membrane of the electric tissue of Electrophorus electricus (L.).

A procedure for the isolation of semi-purified membrane fractions containing nicotinic cholinergic receptors from normal and denervated electric organs of the electric eel was developed. A decrease of the binding capacity of [125I]alpha-bungarotoxin was observed on enriched denervated membrane fractions. After denervation, the acetylcholinesterase activity was significantly smaller than that of the normal tissue. Electron microscopic analysis of the different subcellular fractions was performed both for the normal and denervated tissues. The main alteration observed after denervation was a degeneration of the vesicular structures of toxin binding fractions.

Animals↗
PubMed2006

Normal distribution of presenilin-1 and nicastrin in skeletal muscle and the differential responses of these proteins after denervation.

Presenilin-1 and nicastrin, two components of gamma-secretase associated with Alzheimer's disease plaques, are present in the synapses of the brain and in various peripheral organs, including skeletal muscle. In the present study, we examined the expression pattern of presenilin-1 and nicastrin in normal and denervated hindlimb muscles of the rat. Using immunohistochemical approaches, we found that presenilin-1 and AChRalpha was co-localized at the neuromuscular junction in the normal skeletal muscles of rats. The immunoreactivities of both presenilin-1 and nicastrin were also observed at the sarcolemma of muscle fibers. We discovered that presenilin-1 mRNA and its protein are upregulated after denervation of the soleus and tibialis anterior muscles. Furthermore, clear co-localization between presenilin-1 and DAPI, but not nicastrin, was noted in several myonuclei in the denervated muscles. We recognized a few fibers possessing both ubiquitin and presenilin-1 protein in the cytosol. The amount of presenilin-1 in the nucleus and membrane fraction was more abundantly expressed in the denervated muscle fibers. In contrast, no significant difference in the nicastrin protein level was observed between normal and denervated muscle fibers. These data suggest that enhanced presenilin-1 protein may play a role in the degeneration and regeneration of skeletal muscle.

Amyloid Precursor Protein Secretases↗