Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.1.1.7 (acetylcholinesterase)
 28,390 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

According to our present knowledge of the neuromuscular innervation of the intrinsic laryngeal muscles, the cricothyroid muscle is innervated by the external branch of the superior laryngeal nerve (NLS), whereas all other remaining muscles get their supply from the inferior laryngeal (recurrent) nerve. Mainly in the phoniatric literature, however, opinions differ concerning an additional motoric laryngeal innervation. In human larynges, excised for large unilateral carcinoma, horseradish peroxidase (HRP) was injected into the internal branch of the NLS. Anterograde labelling of axons was demonstrated histochemically. In adjacent sections of the different muscles, end plates and axons were stained histochemically with silver impregnation and acetylcholinesterase. Evidence is presented of motor innervation of the internal branch of the NLS in some laryngeal muscles. With retrograde HRP-tracing in sheep, motoneurons were detected in the nucleus ambiguus, although the recurrent nerve and the external branch had been divided and excised. Thus, histologically an additional neuromuscular supply via the internal branch of the NLS is demonstrated.
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PMID:[Auxiliary motor innervation of the laryngeal muscles via the internal branch of the superior laryngeal nerve]. 304 25

This experiment was designed to test the hypothesis that in the presence of regenerating nerve fibers long-term denervated skeletal muscle does not become reinnervated. This hypothesis was tested in rats by the transplantation of 22-month denervated extensor digitorum longus (EDL) muscles into the sites of EDL muscles in the contralateral, normally innervated legs. Two months after transplantation, the muscles contracted when stimulated via the motor nerve, and based on silver-acetylcholinesterase staining, all grafts possessed innervated motor end plates. Compared to values for control EDL muscles in old rats, the maximum force developed by standard free grafts in old rats was 19% and that of long-term denervated grafts was 7%. For standard free grafts, nerve stimulation produced a maximum force that was 81% of that produced by direct stimulation, and for control EDL muscles in young and old rats, the values were 96 and 90%, respectively. These results show that after long-term denervation rat muscles are capable of becoming functionally reinnervated, even though by the time of reinnervation the animals have attained an advanced age of 26 months.
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PMID:Reinnervation of long-term denervated rat muscle freely grafted into an innervated limb. 318 52

The ability of axons to grow or sprout can vary considerably. In this study we have examined the relation between axon length and the abundance of outgrowth from motor nerve terminals in vivo. Outgrowth from nerve terminals was evoked using botulinum toxin. Terminal axons, sprouts and neuromuscular junctions were visualized using a cholinesterase-silver stain. The amount of axonal outgrowth was compared in several proximal (e.g. rhomboid and paraspinous), intermediate, and distal (e.g. soleus and foot) muscles. Our results show that sprouting is generally more abundant in proximal than in distal muscles. There is a significant inverse correlation between nerve length and the abundance of sprouting from terminal axons. Thus, terminals of short axons appear to have more ability or potential to sprout than those of long axons.
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PMID:Motor nerve outgrowth: reduced capacity for sprouting in the terminals of longer axons. 319 14

Kainic acid was injected bilaterally (4.8 micrograms in 1.2 microliter each side) into the dorsolateral pontomesencephalic tegmentum of cats in order to destroy cholinergic cells which are located within the pedunculopontine tegmental (PPT), laterodorsal tegmental (LDT), parabrachial (PB), and locus ceruleus (LC) nuclei in this species. The neurotoxic lesions resulted in the destruction of the majority (approximately 60%) of choline acetyltransferase (ChAT)-immunoreactive neurons and a minority (approximately 35%) of tyrosine hydroxylase (TH)-immunoreactive neurons, as well as in the destruction of other chemically unidentified neurons, in the region. The effects of these lesions upon the cholinergic innervation of the brain were investigated by comparison of brains with and without lesions which were processed for acetylcholinesterase (AChE) silver, copper thiocholine histochemistry and ChAT radio-immunohistochemistry. In the forebrain, a major and significant decrease in AChE staining, measured by microdensitometry, and associated with a decrease in ChAT immunoreactivity was found in certain thalamic nuclei, including the dorsal lateral geniculate, lateral posterior, pulvinar, intralaminar, mediodorsal and reticular nuclei. All of these nuclei receive a rich cholinergic innervation evident in both AChE histochemistry and ChAT immunohistochemistry. No significant difference in AChE staining or ChAT immunoreactivity was detected in other thalamic nuclei or in the subthalamus, hypothalamus or basal forebrain. In the brainstem, a significant decrease of AChE staining and ChAT immunoreactivity was found in the superior colliculus and the medullary reticular formation, where ChAT-immunoreactive fibers were moderately dense in the normal animal. These results indicate that the pontomesencephalic cholinergic neurons may influence the forebrain by major projections to the thalamus, involving both relay and non-specific thalamocortical projection systems, and thus act as an integral component of the ascending reticular system. They may influence the brainstem by projections onto deep tectal neurons and other reticular neurons, notably those in the medullary reticular formation, and thus also affect bulbar and bulbospinal systems.
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PMID:Neurotoxic lesions of the dorsolateral pontomesencephalic tegmentum-cholinergic cell area in the cat. I. Effects upon the cholinergic innervation of the brain. 325 79

Motor nerve terminal outgrowth (NTO) at neuromuscular junctions (NMJs) occurs rapidly in response to denervation changes in muscle. We have previously found that NTO can produce an elongation of the synaptic area of the NMJ as defined by cholinesterase-silver staining. In the present study, we examined the effects of NTO on a postsynaptic muscle membrane component, the usually stable cluster of acetylcholine receptors (AChRs) at the NMJ. NTO was evoked in rat soleus muscles using botulinum toxin. AChRs were demonstrated using immunocytochemistry or autoradiography of alpha-bungarotoxin binding. Our results show that NTO induces rapid elongation of the cluster of AChRs at the NMJ within 7 d of treatment with botulinum toxin. The growth in the size of the AChR clusters was accompanied by an increase in the number of AChRs/NMJ. No elongation of AChR clusters was seen following surgical denervation, suggesting that cluster growth is related to NTO and not to denervation changes in muscle per se. Growth of NMJ-AChR clusters appeared to result primarily from 2 processes: insertion of new AChRs into the NMJ membrane and, surprisingly, redistribution of preexisting NMJ-AChRs. These results show that NTO can cause rapid changes in the normally stable cluster of AChRs at the NMJ. Motor nerve terminals provide a strong and anatomically precise control of AChRs at the NMJ.
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PMID:Mechanisms of postsynaptic plasticity: remodeling of the junctional acetylcholine receptor cluster induced by motor nerve terminal outgrowth. 330 23

The topographic distribution of specifically labeled neurotensin binding sites was examined by light microscopic radioautography in rat brain sections incubated with monoiodo [125I]Tyr3-neurotensin. Preliminary experiments indicated that under the present experimental conditions [125I]neurotensin specifically binds to a single apparent population of sites with a dissociation constant of 7.7 +/- 0.3 nM, and that fixation of the labeled sections with glutaraldehyde ensures regionally proportional retention of more than 70% of bound [125I]neurotensin molecules. High concentrations of [125I]neurotensin binding sites were detected in the olfactory bulb and tubercle, parts of the neocortex, the lateral septum, the diagonal band of Broca, the caudate putamen, the amygdala, the dentate gyrus, the anterior dorsal nucleus of the thalamus, the suprachiasmatic nucleus of the hypothalamus, the medial habenula, the zona incerta, the substantia nigra and the ventral tegmental area. In certain areas, such as in the diagonal band of Broca, the substantia innominata, the nucleus basalis and the pars compacta of the substantia nigra, discrete accumulations of silver grains were apparent over neuronal perikarya and their proximal dendrites. In most areas, however, the label appeared more or less uniformly distributed over nerve cell bodies and surrounding neuropil. In several instances, the labeling conformed with the distribution of cell bodies of origin and terminal aborizations of specific projection systems, suggesting that neurotensin receptors might be distributed both proximally and distally on the plasma membrane of certain neurons. Such putative "neurotensinoceptive" projection systems might involve part of the mesostriatal, mesocortical and mesolimbic dopamine systems, as well as the raphe-prosencephalic serotonin system and the habenulo-interpeduncular and basal forebrain-cortical cholinergic systems. Finally, areas of dense [125I]neurotensin labeling often corresponded to zones previously shown to exhibit intense acetylcholinesterase staining, suggesting the existence of a possible link between the expression of neurotensin binding sites and that of acetylcholinesterase in certain neuronal populations.
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PMID:Distribution of neurotensin binding sites in rat brain: a light microscopic radioautographic study using monoiodo [125I]Tyr3-neurotensin. 331 97

Rats labelled with [3H]thymidine on embryonic day 15 were treated postnatally with diisopropylfluorophosphate and 2-3 h later perfused with 10% buffered formalin. Cryostat sections of the basal forebrain were autoradiographed and subsequently stained for acetylcholinesterase (AChE). It was shown that this procedure did not significantly influence either the AChE activity or the silver grains over [3H]thymidine-labelled nerve cell nuclei. The labelling index evaluated in cholinergic forebrain regions (medial septum, diagonal band of Broca, substantia innominata, nucleus basalis of Meynert) indicated a caudorostral gradient of the formation of AChE-containing neurons while formation of non-cholinergic neurons showed a more even pattern.
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PMID:A combined method of acetylcholinesterase histochemistry and [3H]thymidine autoradiography: application to neurogenesis of the rat basal forebrain cholinergic system. 341 49

The proportion of polyneuronal innervation was evaluated electrophysiologically in curare-blocked frog cutaneous pectoris muscles after local injury to the muscle fibres on one side. Focal polyneuronal innervation was revealed by recording end-plate potentials evoked by a gradual increase in the stimulus intensity applied to the motor nerve. An increase in the proportion of focally polyneuronally innervated muscle fibres appeared in the injured muscle 3-5 days after injury. The difference between the values obtained 3-5 days and 7-9 days (31 and 38%, respectively) and the control value (18%) was highly significant. A similar increase in the proportion of pluri-innervated muscle fibres was observed in the contralateral muscle, but after a longer period. The different components of complex end-plate potentials (e.p.p.s) usually had similar latencies and rise times in control and experimental muscles. This may indicate that the axons had similar conduction velocities and that synapses were located close to each other. A repeated muscle fibre section 24 h after the initial injury resulted in an enhanced polyneuronal innervation (52%) 7-9 days after the first section. The experiments were repeated on partially blocked muscles in order to detect small e.p.p.s with an amplitude similar to that of spontaneous miniature end-plate potentials (m.e.p.p.s). The proportion of polyneuronally innervated fibres estimated by this technique in control muscles approximated 40%. Polyneuronal innervation was also found to be significantly increased in cut muscles 7-9 days after muscle injury and a week later in contralateral muscles. Combined silver and cholinesterase staining was used to detect morphologically polyneuronal innervation. The comparison of morphological and electrophysiological data indicated that the increase in polyneuronal innervation after muscle injury is likely due to nerve sprouting and formation of new synapses. The results suggest that the signal for nerve sprouting originates from the damaged muscle cell and that it is transferred transneuronally to the contralateral side.
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PMID:Increase in polyneuronal innervation in frog muscle after muscle injury. 348 69

The terminal nerve is composed of a morphologically heterogeneous population of unipolar, bipolar and multipolar neurons located in the nasal and intracranial cavities of vertebrates. The question has arisen as to whether these neurons are neurochemically heterogeneous and therefore possibly functionally different as well. Among the substances localized in the terminal nerve are acetylcholinesterase and luteinizing hormone-releasing hormone-like immunoreactive material. We have developed a double-label procedure, combining immunocytochemistry and enzyme histochemistry to determine whether these two substances are localized within different populations of terminal nerve neurons. Compatibility of the two procedures was accomplished by modifications of the fixative and primary antibody solutions. In the immunocytochemical step, the avidin-biotin-peroxidase complex coupled to a new chromogen, Chromo-red, produced a bright red reaction product in neurons containing luteinizing hormone-releasing hormone-like material. This reaction product was easily differentiated from the black silver-intensified acetylcholinesterase label. In both neonatal and adult preparations, a large population of terminal neurons contained the acetylcholinesterase label only, whereas a smaller population contained both acetylcholinesterase and luteinizing hormone-releasing hormone-like material. The acetylcholinesterase-containing population of neurons was concentrated peripherally and included multipolar neurons. In contrast neurons with the two substances co-localized were unipolar or bipolar and were concentrated centrally. The simultaneous visualization of acetylcholinesterase and luteinizing hormone-releasing hormone-like material in the same tissue section enable the differentiation of two separate neurochemically defined populations of terminal neurons. The distribution of these two neuronal types was the same in neonatal and adult animals. These data provide support for a functional diversity of terminal neurons.
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PMID:Acetylcholinesterase and luteinizing hormone-releasing hormone distinguish separate populations of terminal nerve neurons. 354 Jul 22

The mdx mutant mouse was first observed during a survey of genetic variations of pyruvate kinase in the mouse. Affected mice have high serum levels of this enzyme and although showing little disability they have widespread and severe muscle disease. Light and electron microscopy, muscle enzyme histochemistry and combined cholinesterase-silver impregnations were used for the study of affected and control animals aged 1 day to 1 year. An early ultrastructural abnormality present already at 1 day was scattered focal streaming of Z-lines. Later there was also segmental muscle fibre necrosis and regeneration. The proportion of muscle fibres showing either necrosis, regeneration or internal nuclei was assessed in several muscles, at ages ranging from 10 days to 1 year. Acute segmental necrosis and regeneration were most marked at 1 to 2 months, although they were present at all ages. The number of fibres with internal nuclei increased progressively until 3 months when 70-80% showed this abnormality. Nerve terminals were unaffected but there was a reduction in the number and depth of postsynaptic folds at motor end-plates in adult animals, confirmed by morphometric analysis. Quantitative study of L4 motor root and tibial nerve showed that fibre numbers, axonal calibres and myelin sheath thickness were normal at all ages. No qualitative abnormalities were found in the CNS or other organs. The findings strongly suggest that the mdx mutant has a primary muscle disease and that the nervous system is normal.
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PMID:The mutant mdx: inherited myopathy in the mouse. Morphological studies of nerves, muscles and end-plates. 356 25


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