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 1,711 records · Page 95Linked to original sources
PubMedDate not supplied

Phosphorylation of the sarcolemma of dystrophic and normal hamster muscle following denervation.

The rapid phosphorylation at 0 degree C of sarcolemma preparations of hamster leg muscle was compared with (Na+,K+)-ATPase activity in sham-operated and 7-day denervated muscle. The phosphorylation appeared to be under the trophic influence of the sciatic nerve since the denervated preparations exhibited a markedly reduced phosphorylation. In similar studies using dystrophic hamsters the sarcolemma preparations from sham-operated and denervated leg muscle both exhibited the same degree of phosphorylation.

Animals↗
PubMed1983

Effect of parasympathetic denervation on acetylcholine levels in the rat parotid gland. Is there an extraneuronal pool of acetylcholine?

Parasympathetic denervation of the rat parotid gland by avulsion of the auriculotemporal nerve caused a marked and lasting decrease in gland weight. Parasympathectomy did not change the levels of choline in the gland but decreased by 60% the levels of acetylcholine (ACh) ten days after surgery and 65% at 28 days. It is puzzling that relatively high levels of ACh remained after parasympathetic denervation. The presence of additional cholinergic nerves that innervate the gland, or pass through it en route to other structures may account for some of the remaining ACh. Also, Schwann cells from denervated nerves might have contributed to some of the ACh. The existence of an extraneuronal source of ACh is considered.

Acetylcholine↗
PubMed1982

Effects of denervation on the sensitizing effect to noradrenaline induced by morphine in the vas deferens of mice treated chronically with morphine.

The acute administration of morphine to the isolated vas deferens from mice chronically exposed to this analgesic, induced a facilitatory effect on the responses of the muscle to exogenous noradrenaline. It has been suggested that this sensitizing property of morphine might reflect a dependence-like state of the vas deferens. In the present paper, the capability of met- and leu-enkephalin to substitute for morphine was studied, as well as the influence of innervation on the apparent dependence state. The contractile responses to noradrenaline and to acetylcholine were increased after the administration of morphine to the bath containing a denervated vas deferences, prepared from chronically morphinized mice. Morphine administration facilitated noradrenaline- but not acetylcholine-induced contractile effects in vas deferens isolated from mice which had been chronically treated with either morphine or morphine plus guanethidine. The presence of met- or leu-enkephalin in the isolated vas deferens from chronically morphinized mice (either intact, denervated or treated with guanethidine) failed to sensitize contractile responses to noradrenaline or acetylcholine. It is concluded that (a) the sensitizing effect induced by morphine in the vas deferens from mice chronically treated with morphine is specific for the adrenergic neurotransmitter; (b) the effect of morphine is not mimicked by opiate peptides; and (c) denervation of the vas deferens of mice treated chronically with morphine does not suppress the noradrenaline-sensitizing property of morphine.

Acetylcholine↗
PubMed1993

Effect of medullary lesions, vagotomy and carotid sinus denervation on fetal breathing.

Chronically prepared fetal sheep were subjected to bilateral surface lesions of the Area "S" on the ventrolateral medulla and/or to peripheral chemoreceptor denervation by section of the vagus, sinus or both nerves. Sino-aortic denervation or Area "S" lesions reduced the incidence of fetal breathing (FB) for several days. Area "S" lesions also disrupted the pattern of FB; diaphragmatic EMG activity initially was mostly tonic and then of very high frequency, up to 7 Hz. Incidence and pattern of FB generally recovered by 7 days, but mean Ti was reduced in Area "S" lesioned fetuses (0.14 +/- 0.01 sec) compared to nonlesioned fetuses (0.19 +/- 0.01 sec) (P < 0.0001). Respiratory sensitivity to CO2 was variable but not different between control, denervated, and Area "S" lesioned groups. Eight of eight fetuses with Area "S" lesions were unable to initiate breathing at birth, but three sham operated fetuses were born normally. These data suggest that the classical peripheral and central chemoreceptors have a negligible influence on the control of FB, and that breathing activity in the fetus is mediated by a different mechanism than during postnatal life.

Animals↗
PubMed1986

Increase in beta- and alpha 1-adrenoceptor binding sites in the rat brain and in the alpha 1-adrenoceptor functional sensitivity after the DSP-4-induced noradrenergic denervation.

Changes in the density of beta- and alpha 1-adrenoceptors were studied following denervation of the rat cerebral cortex and hippocampus, caused by systemic administration of DSP-4. The noradrenergic denervation increased both beta- and alpha 1-adrenoceptor density by about 30 and 17%, respectively in the cortex, and by about 30% in the hippocampus. In order to estimate the behavioral response of normal and DSP-4-treated rats to alpha 1-agonist, the influence of phenylephrine (25 micrograms ICV) on the exploratory activity of rats in the open field was measured. Phenylephrine failed to change the exploratory activity of normal rats, but significantly increased it in DSP-4 animals. The results indicate that noradrenergic denervation produces an increase in number of both beta- and alpha 1-adrenoceptors and the functional supersensitivity to the alpha 1-adrenergic agonists.

Animals↗
PubMed1985

Effects of renal denervation on renin release induced by intracerebroventricular administration of biological active peptides in conscious rats.

Experiments were performed to determine whether the renal nerve mediates the renin release induced by intracerebroventricular administration of angiotensin II (ANG II), bradykinin (BK), leucine-enkephalin (Leu-ENK) and neurotensin (NT). In sham-operated rats, both ANG II and NT suppressed plasma renin activity (PRA), BK did not affect PRA, and Leu-ENK increased PRA. Renal denervation abolished the increase in PRA by Leu-ENK. Suppression of PRA by ANG II was attenuated in denervated rats. Renal denervation did not influence the renin release by BK or NT. These results suggest that the renal nerve plays an important role in elevating PRA after central stimulation by Leu-ENK. Although suppression of PRA is mainly mediated by mechanisms other than the renal nerve, the renal nerve partially participates in suppression of PRA by ANG II.

Angiotensin II↗
PubMed1991

The ACTH-(4-9) analogue ORG 2766 facilitates denervation supersensitivity after a unilateral 6-OHDA lesion of the corpus striatum in rats.

UNLABELLED: Direct bilateral 6-OHDA lesioning of the nucleus accumbens causes a temporary reduction in motility, followed by a spontaneous recovery in 3-4 weeks. The ACTH-(4-9) analogue ORG 2766 shortens this period to 1 week. The functional and the peptide-induced facilitation of recovery are accompanied by enhanced motility upon administration of the dopamine agonist apomorphine which may be related to denervation supersensitivity. The present experiments were performed to investigate the interaction between ORG 2766 and denervation supersensitivity in another dopaminergic terminal area i.e. the corpus striatum. After a unilateral 6-OHDA lesion of the right corpus striatum, contralateral rotation was observed upon administration of a high dose of apomorphine 2, 3 and 4 weeks after the lesion, indicating supersensitivity of postsynaptic dopaminergic receptor systems. Contralateral rotation upon administration of this dose of apomorphine was observed in ORG 2766 treated animals, already at 1 week after the lesion. Peptide treatment resulted in an enhanced sensitivity for apomorphine, since contralateral rotation was observed in peptide but not in placebo treated, 6-OHDA lesioned animals after a low dose of apomorphine. IN CONCLUSION: treatment with ORG 2766 facilitates the development of denervation supersensitivity and enhances sensitivity for apomorphine probably through an increased affinity of dopaminergic receptors for dopamine agonists.

Adrenocorticotropic Hormone↗
PubMed1984

The effect of intraportal and intravenous glucose infusion and an intravenous glucose tolerance test on insulin and glucagon levels in conscious cats with normal and chronically phenol-denervated livers.

Cats were prepared with chronically implanted catheters in the portal and femoral vein for administration of glucose. A femoral arterial catheter was used for blood sampling. After at least 5 days following the implantations, cats received an infusion of 3 mg/kg/min into the portal vein and the insulin and glucagon responses were compared with a similar infusion into the femoral vein. The hypothesis predicted that glucose receptors in the liver would result in greater pancreatic hormonal responses than would be seen with the femoral infusions of glucose. This did not occur. There was no statistically significant difference between the rise in insulin and the decrease in glucagon elicited by the glucose infusion into the two alternate infusion sites. A sham-denervated series showed similar responses. A group of cats that underwent hepatic denervation using topical phenol application to the hepatic plexus near the hilum of the liver was tested. The responses of the denervated group were similar to those for the control and sham-operated groups, confirming that hepatic glucose receptors do not serve as an afferent limb of a hepato-pancreatic reflex controlling insulin and glucagon release in conscious cats. In all experiments, a bolus of glucose (500 mg) was injected i.v. to represent a tolerance test. The responses of blood glucose levels, pancreatic insulin and glucagon and recovery from the stimulus were similar in all groups which suggests that hepatic nerves are not essential for a normal hepatic response to intravenously infused glucose. It is suggested, however, that hepatic nerves may be important in producing normal hepatic responses to oral glucose loads.

Animals↗
PubMed1991

Sprouting of aberrant neuropeptide Y-immunoreactive sympathetic nerves into neonatally denervated smooth muscle.

Sympathetic nerves normally project ipsilaterally to lateral cranial targets. Following unilateral superior cervical ganglionectomy in neonatal rats, however, neurons from the contralateral superior cervical ganglion sprout into the denervated region. In the present study we examined neuropeptide Y immunoreactivity (NPY-ir) of neurons comprising ipsilateral (control) and denervation-induced contralateral pathways to the superior tarsal smooth muscle of the eyelid. Fluoro-Gold injection of the control muscle retrogradely labelled 133 +/- 18 neurons in the ipsilateral superior cervical ganglion; of these, 21 +/- 3% displayed detectable NPY-ir. Fluoro-Gold injections of the reinnervated muscle labelled 20 +/- 4 neurons in the contralateral superior cervical ganglion, of which 85 +/- 3% contained detectable NPY-ir. Examination of the control tarsal muscle revealed DBH-ir noradrenergic nerves throughout the muscle and vasculature, while NPY-ir nerves were present primarily around blood vessels. In the reinnervated preparation, NPY-ir fibers innervated both blood vessels and tarsal muscle in a pattern similar to that of DBH-ir innervation. Acute excision of the remaining superior cervical ganglion eliminated all DBH-ir fibers bilaterally; NPY-ir was reduced markedly in the reinnervated preparations, though some fibers remained. We conclude that, following neonatal denervation, the tarsal muscle is reinnervated by a subpopulation of sympathetic neurons that differs in neuropeptide phenotype from that of the normal ipsilateral innervation.

Animals↗
PubMed1996

Developmental and denervation changes in c-ret proto-oncogene expression in chick motoneurons.

Receptor tyrosine kinases (RTKs) play important roles in cellular differentiation, survival, and proliferation. To search for genes involved in the survival of motoneurons, we isolated the RTKs specifically expressed on them. We used RT-PCR, by which RNA was obtained from purified embryonic day 5 (E5) chick motoneurons, and screened by in situ hybridization. Of 17 RTK cDNA clones, c-ret expression gradually increased in the motoneurons of the spinal cord during development. Compared with the expression of the neurotrophin receptor, TrkC, that of c-ret was very high in motoneurons from around E17 to adulthood. The level of c-ret expression on the motoneurons was unaffected by deafferentation at E2, but changed after denervation at post-hatching day 2. The in situ hybridization signal for c-ret mRNA increased slightly at day 1, then decreased progressively up to day 8, and increased again 2 weeks after sciatic nerve denervation in the motoneurons of the lumbar spinal cord. There were also changes in the signal of the lesioned sciatic nerve. In the most distal part from the lesioned site, the signal for c-ret mRNA significantly increased from day 3 on after denervation. These results suggested that the c-ret gene may encode the receptor for a factor involved in motoneuron differentiation and the promotion of regeneration of injured peripheral nerves.

Amino Acid Sequence↗
PubMedDate not supplied

Alpha- and beta-adrenergic receptors of the rat cerebral cortex and cerebral microvessels in aging, and their response to denervation.

We studied the effects of aging and norepinephrine depletion 2 weeks after unilateral locus ceruleus lesion on alpha 1-, alpha 2- and beta-adrenergic receptors by ligand binding methods in the ipsilateral and contralateral cerebral cortex of Fischer-344 rats. We also studied the effects of aging and noradrenergic denervation on beta-adrenergic receptors in isolated cerebral microvessels. We found that specific [125I]HEAT binding to alpha 1-adrenergic receptors was not affected by aging or by norepinephrine depletion. Although aging also had no effect on the density or affinity of [3H]UK-14,304 and [125I]pindolol binding to alpha 2- and beta-adrenergic receptors, the density of receptors increased significantly in all age groups after noradrenergic denervation. beta-Adrenergic receptors of cerebral microvessels also were unaffected by aging, but increased their density after noradrenergic denervation at all ages. In all instances, there were no significant effects on the affinity of ligand binding. We conclude that aging does not affect the density or the affinity of adrenergic receptors in the cerebral cortex of Fischer-344 rats, nor does it affect the response of these receptors to norepinephrine depletion.

Aging↗
PubMed1986

Calcium-related abnormalities in fast and slow denervated skeletal muscle in rats.

Muscle weights, Ca-ATPase activity and calcium-binding proteins were studied after denervation in rat extensor digitorum longus (EDL) and soleus (Sol) muscles. Muscle weights decreased progressively as a function of denervation time: after 28 days EDL weight diminished by 70% and Sol weight by 47%. Ca-ATPase activity and calsequestrin were quite reduced in control Sol as compared to the control EDL. Denervation caused a considerable reduction in Ca-ATPase and calsequestrin in EDL, making it resemble the control Sol.

Animals↗
PubMed1987

Comparison of red and white muscle wet weight changed by age, denervation and morbid states.

[Na]i, [K]i and wet weight of the extensor digitrum longus (EDL) and soleus (SOL) muscles of 9- and 52-week-old rats were measured for 7 days after sectioning of the sciatic nerve. The changes in wet weight of the EDL and SOL muscles of rats over 52 weeks and those of morbid state rats were also measured. There was no significant difference in wet weights between the EDL and SOL muscles in infant rats, but the EDL muscle became much heavier than the SOL muscle with aging. The decrease in rate of growth of wet weight of the EDL and SOL muscles caused by denervation, was greater in young rats than in mature rats. In addition, the rate of decrease was greater in the SOL muscles than in the EDL muscles in both young and mature rats. The [Na]i increased while [K]i was decreased by denervation, and the net Na+ increase and the net K+ loss were greater in young rats than in mature rats. The changing rate was more remarkable in the EDL muscles than in the SOL muscles throughout the aging process. During DOCA treatment over 4 weeks, the decrease of muscle wet weight was greater in the EDL muscles. The mechanisms which serve to maintain normal muscle wet weight in the SOL muscle after denervation or treatment with DOCA, were discussed.

Aging↗
PubMed1982

Denervation exposes cryptic concanavalin A binding sites in skeletal muscle membranes.

Denervation produces significant changes in glycoproteins on the surfaces of skeletal muscles which can be detected as an increase in membrane-bound carbohydrate and an increase in specific binding of labelled lectins. The increased binding of concanavalin A to denervated membranes is detectable only in intact membranes and is abolished by treatments which disrupt or perturb membrane structure whereas the increased binding of Ricinus communis agglutinin is detectable under both conditions. We suggest that, in addition to chemical modification of existing carbohydrate chains in glycoproteins and the synthesis of new glycoproteins, denervation results in an altered geometric arrangement of existing membrane glycoproteins.

Animals↗
PubMed1987

Striatal adenosine levels measured 'in vivo' by microdialysis in rats with unilateral dopamine denervation.

Adenosine, inosine, hypoxanthine and guanosine were measured in perfusates collected from the right and left striatum of halothane-anaesthetized naive and 6-hydroxydopamine-denervated rats by using microdialysis. Samples were taken under basal and KCl-stimulated conditions. Dopamine, dihydroxyphenylacetic acid (DOPAC), homovanillic acid (HVA) and 5-hydroxyindoleacetic acid (5-HIAA) were simultaneously measured. Purines and monoamines were assayed by HPLC-UV and HPLC-EC respectively. In naive rats, basal adenosine (1 microM), inosine (2 microM), hypoxanthine (4 microM), guanosine (0.5 microM) and dopamine (DA, 0.02 microM) levels (corrected by using the in vitro % recovery of each probe) were increased by the inclusion of 100 mM of KCl into the perfusion medium (2.5-, 3-, 3.5-, 1.5- and 30-fold, respectively, while DOPAC (6 microM), HVA (5 microM) and 5-HIAA (3 microM) levels were (72%, 68% and 45% respectively). DA was strongly diminished in the denervated striatum, but when detectable, could be increased (1- to 12-fold) by KCl stimulation. Adenosine, inosine, hypoxanthine and guanosine were, however, largely unaffected by the DA denervation and could be enhanced by KCl stimulation (2-, 3-, 4- and 1.5-fold respectively). The present results indicate that: (1) as in the case for DA, there is a pool of striatal adenosine which is releasable by high concentrations of extracellular K+; however, (2) this pool of adenosine seems not to be significantly modified by mesencephalic dopamine deafferentation.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1988

Dependence of acetylcholine receptor channel conversion on muscle activity at denervated neonatal rat endplates.

During the development of the motor endplate, the apparent mean open time of the junctional acetylcholine (AChR) channels decreases during the first 3 weeks of postnatal life from about 4 to about 1 ms. This decrease is prevented by early denervation of the muscle, suggesting a neural control of subsynaptic AChR channel properties. To further examine the nature of this neural influence, neonatal rat soleus muscles were now denervated at an early stage of endplate development and the muscles were kept active by chronic stimulations in vivo for 4 days. The gating properties of AChR channels at the denervated endplates and at control endplates of similar age were then examined by analysis of acetylcholine-induced endplate current fluctuations and of the time course of miniature endplate currents, respectively. The results indicate, that stimulation restores the maturation of 'adult' AChR channel properties even in the absence of the nerve, suggesting an important role of muscle activity in synapse development.

Action Potentials↗
PubMed1993

Myenteric neuron number after acute and chronic denervation of the proximal jejunum induced by benzalkonium chloride.

The effects of benzalkonium chloride (BAC) on the number of myenteric neurons after acute (until 10 days after BAC application) and chronic (30 and 60 days after BAC application) denervation of the proximal jejunum were determined in rats. There was a significant reduction in the number of myenteric neurons of all segments treated with BAC. The extent of denervation varied with time, and it was reduced in the denervated segments of the chronic group in comparison with the acute group. This may be due to the neuroplasticity phenomenon appearing during the chronic phase.

Animals↗
PubMed1983

Respiratory activities of subsarcolemmal and intermyofibrillar mitochondrial populations isolated from denervated and control rat soleus muscles.

Ultraturrax and Nagarse released populations of mitochondria isolated from control and day 21 denervated rat soleus muscle were characterized with respect to their oxidative phosphorylation, ADP translocase and ATPase activities. Both Ultraturrax and Nagarse released mitochondrial populations displayed lower capacities for oxidative phosphorylation; lower ADP translocase activities and higher Mg2+ stimulated ATPase activities than their corresponding controls. For both the denervated and control states, the Nagarse-released mitochondrial populations displayed significantly higher respiratory activities than the Ultraturrax released fractions. The significance of these findings is discussed with regard to the process of mitochondrial respiratory control. In addition the role of mitochondrial dysfunction in denervation muscular atrophy is assessed.

Adenosine Triphosphatases↗