Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: 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)

The autonomous innervation of the feline testis was investigated by immunohistochemistry and a modified acetylcholinesterase technique. The nerves reach the testis mainly by two routes: (1) with testicular artery and pampiniform plexus to the cranial extremity (funicular contribution), (2) from the epididymal tail to the caudal extremity (caudal contribution). Within the tunica albuginea the funicular contribution supplies the cranial two thirds, whereas the caudal third of the tunica receives its nerves via the ligamentous connection between testis and epididymal tail. The nerve bundles accompanying the testicular artery give branches to the arterial wall and the pampiniform plexus. When reaching the cranial testicular pole the bundles separate; the majority of them pass into the centrally located mediastinum testis, another large portion enters the tunica albuginea, particularly on its epididymal side. The septula testis are innervated from both sides, that is from the mediastinum and from the tunica albuginea. In the cat, contrary to other mammals, all septula are innervated. Furthermore, nerve fibers occur regularly within the testicular lobules. Generally, the testicular nerves of the cat are unmyelinated and mainly vascular nerves, but fibers are also found within the connective tissue compartments of the testis. The vast majority of all autonomous testicular nerves are postjunctional sympathetic fibers. Terminal ramifications of cholinergic fibers are exclusively observed in the wall of medium-sized arterioles within mediastinum, septula and lobuli testis. Neuropeptide Y is the most frequent peptidergic transmitter in feline testicular vascular plexuses. The amount of calcitonin gene-related peptide-positive fibers is also remarkably high in the testis, but prefers a location within the stroma of the tunica albuginea, mediastinum and septula. In the cat, Leydig cells occur not only in intertubular locations, but also as intratunical and mediastinal Leydig cells. In all three localizations solitary nerve fibers are observed between Leydig cell groups. These fibers are generally dopamin-beta-hydroxylase- and tyrosine hydroxylase-positive, some contain calcitonin gene-related peptide and, very few, substance P.
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PMID:The nerve distribution in the testis of the cat. 1150 54

The innervation of the camel epididymis was studied in 26 apparently healthy, sexually mature animals aged between 4 and 12 years. The material was collected during the different seasons of the year. Generally, five samples were taken from each epididymis. To demonstrate the general innervation pattern, immunohistochemical reactions to protein gene product-9.5, neurofilaments and neuron-specific enolase were used, in addition to acetylcholinesterase histochemistry. The nerve supply of the epididymis comes from two sources: (1) The majority of fibers come from the N. spermaticus inferior and accompany the deferent duct. (2) Another contribution stems from the N. spermaticus superior and enters the head region of the epididymis. From the exterior, the nerves penetrate the capsule of the organ to reach the interductular connective tissue. The terminal ramifications are observed directly within the wall of the duct and the wall of the epididymal arteries. The veins of the camel epididymis are not innervated. In the wall of the ductus epididymidis, the nerve fibers form plexuses at the subepithelial level and in the muscular coat. The amount of nerve fibers increases from the head to the tail, paralleling an increase in the intrinsic musculature. The intramural and interductular innervation of epididymal body and tail shows clear seasonal variations: More fibers and stronger reactions are observed during the winter season; the lowest density and the weakest reactions occur during the summer season. All epididymal nerves of the camel are unmyelinated. The majority of the intramural fibers and all in the arterial wall represent postjunctional sympathetic axons, but in the intramural plexuses of the duct a considerable number of cholinergic fibers are also present. Neuropeptide Y is the most frequent peptidergic transmitter and generally co-localized with dopamine-beta-hydroxylase in the sympathetic axons. Vasoactive intestinal polypeptide has a distribution similar to that of the cholinergic fibers. Calcitonin gene-related peptide-positive axons occur in moderate numbers, but never in the arterial innervation. Together with the relatively rare substance P-containing fibers, the calcitonin gene-related peptide-positive axons seem to represent the only sensory nerves in the camel epididymis.
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PMID:On the intrinsic innervation of the epididymis of the camel (Camelus dromedarius). 1220 Oct 39

MU33, an antibody to calcitonin gene-related peptide (CGRP), was used to investigate the magnitude of CGRP-containing nerve fiber endings, compared to acetylcholinesterase (AChE)-containing nerve fiber endings on outer hair cells (OHCs). Results showed that CGRP-containing nerve fiber immunoreactivity mimicked the AChE fiber OHC staining pattern across the cochlea suggesting that CGRP can function as both a medial efferent (contacting primarily OHCs) and as a lateral efferent (contacting primarily inner hair cell afferents) neurotransmitter.
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PMID:CGRP- and cholinergic-containing fibers project to guinea pig outer hair cells. 1236 63

Hodological, electrophysiological, and ablation studies indicate a role for the basal forebrain in telencephalic vocal control; however, to date the organization of the basal forebrain has not been extensively studied in any nonmammal or nonhuman vocal learning species. To this end the chemical anatomy of the avian basal forebrain was investigated in a vocal learning parrot, the budgerigar (Melopsittacus undulatus). Immunological and histological stains, including choline acetyltransferase, acetylcholinesterase, tyrosine hydroxylase, dopamine and cAMP-regulated phosphoprotein (DARPP)-32, the calcium binding proteins calbindin D-28k and parvalbumin, calcitonin gene-related peptide, iron, substance P, methionine enkephalin, nicotinamide adenine dinucleotide phosphotase diaphorase, and arginine vasotocin were used in the present study. We conclude that the ventral paleostriatum (cf. Kitt and Brauth [1981] Neuroscience 6:1551-1566) and adjacent archistriatal regions can be subdivided into several distinct subareas that are chemically comparable to mammalian basal forebrain structures. The nucleus accumbens is histochemically separable into core and shell regions. The nucleus taeniae (TN) is theorized to be homologous to the medial amygdaloid nucleus. The archistriatum pars ventrolateralis (Avl; comparable to the pigeon archistriatum pars dorsalis) is theorized to be a possible homologue of the central amygdaloid nucleus. The TN and Avl are histochemically continuous with the medial aspects of the bed nucleus of the stria terminalis and the ventromedial striatum, forming an avian analogue of the extended amygdala. The apparent counterpart in budgerigars of the mammalian nucleus basalis of Meynert consists of a field of cholinergic neurons spanning the basal forebrain. The budgerigar septal region is theorized to be homologous as a field to the mammalian septum. Our results are discussed with regard to both the evolution of the basal forebrain and its role in vocal learning processes.
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PMID:Organization of the avian basal forebrain: chemical anatomy in the parrot (Melopsittacus undulatus). 1245 5

The calcitonin gene-related peptide (CGRP) is released by motor neurons where it exerts both short and long term effects on skeletal muscle fibers. In addition, sensory neurons release CGRP on the surrounding vasculature where it is in part responsible for local vasodilation following muscle contraction. Although CGRP-binding sites have been demonstrated in whole muscle tissue, the type of CGRP receptor and its associated proteins or its cellular localization within the tissue have not been described. Here we show that the CGRP-binding protein referred to as the calcitonin receptor-like receptor is highly concentrated at the avian neuromuscular junction together with its two accessory proteins, receptor activity modifying protein 1 and CGRP-receptor component protein, required for ligand specificity and signal transduction. Using tissue-cultured skeletal muscle we show that CGRP stimulates an increase in intracellular cAMP that in turn initiates down-regulation of acetylcholinesterase expression at the transcriptional level, and, more specifically, inhibits expression of the synaptically localized collagen-tailed form of the enzyme. Together, these studies suggest a specific role for CGRP released by spinal cord motoneurons in modulating synaptic transmission at the neuromuscular junction by locally inhibiting the expression of acetylcholinesterase, the enzyme responsible for terminating acetylcholine neurotransmission.
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PMID:Localization of the calcitonin gene-related peptide receptor complex at the vertebrate neuromuscular junction and its role in regulating acetylcholinesterase expression. 1270 85

Posterior urethral valves (PUV) are the most common cause of bladder outlet obstruction (BOO) in infancy. Bladder instability, poor compliance and myogenic failure are responsible for the poor long-term prognosis in these patients. Previous studies have reported abundance of sensory neuropeptides, e.g. substance P (SP), calcitonin gene-related peptide (CGRP), vasoactive intestinal polypeptide (VIP) and acetylcholinesterase (AchE) nerves in the urinary bladder. We hypothesized that the functional changes in the bladder following BOO are due to alteration in cholinergic and sensory neuropeptide innervation. We therefore investigated cholinergic and sensory innervation of urinary bladder following BOO. Fifteen immature male guinea pigs (Hartley strain) 3-4 weeks old and weighing approximately 250 g. underwent placement of a silk ligature around the bladder neck to induce BOO. Controls included 5 sham-operated animals. The animals were killed 1, 2 and 4 weeks following obstruction, respectively. Whole-mount preparation and conventional sections of bladder wall were performed. AchE histochemistry, and single-label immunofluorescence histochemistry for SP, CGRP and VIP were utilized. Light microscopy and laser scanning confocal microscopy were used to assess the results. AchE staining showed marked increase in cholinergic innervation density within the suburothelial region following BOO. The staining for SP, CGRP and VIP demonstrated marked reduction in sensory nerve density within the suburothelial region 1 week following BOO and the lack of sensory innervation 4 weeks after BOO. The marked reduction in sensory innervation of the bladder and simultaneous increase in cholinergic innervation following BOO may lead to bladder instability and decrease in bladder compliance.
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PMID:Alterations in cholinergic and neuropeptide innervation of urinary bladder following partial bladder outlet obstruction. 1275 93

This work addresses the presence, pharmacological properties, and anatomical localization of calcitonin gene-related peptide-alpha (CGRPalpha) binding sites and the receptor's accessory proteins in endplate-enriched and non-endplate muscle membrane samples from adult rat gracilis muscles. We examined the binding of (125)I-[Tyr(0)]-CGRPalpha, the competitive binding of CGRPalpha analogs, the immunohistochemical localization of the receptor's accessory proteins, and Western blots of the receptor component protein. Results show that: (a). (125)I-[Tyr(0)]-CGRPalpha binding is saturable, specific, and consistent with the presence of a homogeneous population of binding sites (Hill coefficients=1.0) in endplate and non-endplate samples exhibiting dissociation constants of 0.39 nM and 0.38 nM, respectively; (b). the density of binding sites in the endplate samples (71.0 fmoles/mg protein) is considerably higher than that in their non-endplate counterparts (34.6 fmoles/mg protein); (c). unlabeled CGRPalpha, hCGRP8-37 and calcitonin compete with the radioligand with the same order of potency in the endplate and non-endplate samples; and (d). the localization of the receptor accessory proteins, including the receptor activity-modifying protein (RAMP1) and the receptor component protein (RCP), for the most part matches that of the motor end-plates. Thus, gracilis muscles express CGRPalpha-specific binding sites which are predominantly localized in the muscle's motor endplate regions where RAMP1, RCP, CGRPalpha, acetylcholine receptors, and acetylcholinesterase are detected in high concentrations. These findings imply that the CGRPalpha binding sites reflect the presence of physiologically functional receptors with a pharmacological profile consistent with that of the CGRPalpha receptor type 1 (CGRP1). When considered together with earlier studies on the same neuromuscular preparation, the present work further suggests that the motoneuron-dependent trophic control of acetylcholine receptors and acetylcholinesterase in skeletal muscle endplates is partly mediated by nerve-derived CGRPalpha activating specific receptors which are highly sensitive to the truncated peptide hCGRP8-37.
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PMID:Calcitonin gene-related peptides: their binding sites and receptor accessory proteins in adult mammalian skeletal muscles. 1277 May 50

Presynaptic motor neuron synthesizes and secretes acetylcholinesterase (AChE) at vertebrate neuromuscular junctions. In order to determine the retrograde role of muscle in regulating the expression of AChE in motor neuron, a chimeric co-culture of NG108-15 cell, a cholinergic cell line that resembles motor neuron, with chick myotube was established to mimic the neuromuscular contact in vitro. A DNA construct of human AChE promoter tagged with luciferase (pAChE-Luc) was stably transfected into NG108-15 cells. The co-culture with myotubes robustly stimulated the promoter activity as well as the endogenous expression of AChE in pAChE-Luc stably transfected NG108-15 cells. Muscle extract derived from chick embryos when applied onto pAChE-Luc-expressing NG108-15 cells induced expressions of AChE promoter and endogenous AChE. The cAMP-responsive element mutation on human AChE promoter blocked the muscle-induced AChE transcriptional activity in cultured NG108-15 cells either in co-culturing with myotube or in applying muscle extract. The accumulation of intracellular cAMP and the phosphorylation of cAMP-responsive element-binding protein in cultured NG108-15 cells were stimulated by applied muscle extract. Part of the muscle-induced signaling was mimicked by application of calcitonin gene-related peptide in cultured NG108-15 cells. These results suggest the muscle-induced neuronal AChE expression in the co-culture is mediated by a cAMP-dependent signaling.
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PMID:Muscle induces neuronal expression of acetylcholinesterase in neuron-muscle co-culture: transcriptional regulation mediated by cAMP-dependent signaling. 1296 41

Small-diameter sensory nerves innervating the skin are responsive to noxious stimuli, and an injury to these nerves is presumably related to neuropathic pain. Injury-induced neuropathic pain in animals can be produced by laser irradiation, which usually requires concomitant use of photosensitive dyes, known as the photochemical approach. It is not clear whether laser irradiation alone can induce neuropathic pain. In addition, two issues are important to apply these approaches: the relationship between the extent of laser irradiation and the occurrence of neuropathic pain, and the susceptibility of small-diameter sensory nerves in the skin to laser-induced neuropathic pain. To address these issues, we designed a new model of focal neuropathy by applying a diode laser of 532 nm (100 mW) to the sciatic nerve and evaluated small-diameter nerves by quantifying skin innervation and large-diameter nerves by measuring amplitudes of the compound muscle action potential (CMAP). Immediately after laser irradiation, epineurial vessels were occluded due to the formation of thrombi, and the blood flow through these vessels was markedly reduced. On postoperative day (POD) 2, animals developed characteristic manifestations of neuropathic pain, including spontaneous pain behaviors, thermal hyperalgesia, and mechanical allodynia. These phenomena peaked during PODs 7-21, and lasted for 3-6 weeks. The neuropathology at the irradiated site of the sciatic nerve included a focal area of axonal degeneration surrounded by demyelination and endoneurial edema. The extent of damage to large-diameter motor and sensory nerves after laser irradiation was evaluated by nerve conduction studies. On the irradiated sides, amplitudes of the compound muscle action potentials and sensory nerve action potentials (SNAPs) were reduced to 65.0% (P < 0.0001) and 42.5% (P < 0.01) of those on the control sides, respectively. Motor innervation of the neuromuscular junctions (NMJs) on plantar muscles was examined by combined cholinesterase histochemistry and immunohistochemistry. The ratio of innervated NMJs on the operated sides decreased to 76.3% of that on the control side. Skin innervation in the territory of the irradiated sciatic nerves was evaluated by immunohistochemistry with neuronal markers. Among these markers, epidermal nerve densities for protein gene product (PGP) 9.5, calcitonin gene-related peptide (CGRP), and substance P (SP) were significantly lower on the irradiated sides than the control sides with a different degree of loss for each marker (42.1-53.1%, P < 0.05). Results suggest that laser-induced focal neuropathy provides a new system for studying neuropathic pain. With this approach, the extent of nerve injury can be quantified. Both small-diameter epidermal nerves and large-diameter sensory and motor nerves are susceptible to laser-induced injury of different degrees.
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PMID:Skin denervation, neuropathology, and neuropathic pain in a laser-induced focal neuropathy. 1564 95

Previously, a novel tight junction modulating (TJM) peptide was described affording a transient, reversible lowering of transepithelial electrical resistance (TER) in an in vitro model of nasal epithelial tissue. In the current report, this peptide has been further evaluated for utility as an excipient in transepithelial drug formulations. Chemical stability was optimal at neutral to acidic pH when stored at or below room temperature, conditions relevant to therapeutic formulations. The TJM peptide was tested in the in vitro tissue model for potential to enhance permeation of a low-molecular-weight (LMW) drug, namely the acetylcholinesterase inhibitor galantamine, as well as three peptides, salmon calcitonin, parathyroid hormone 1-34 (PTH(1-34)), and peptide YY 3-36 (PYY(3-36)). In all cases, the TJM peptide afforded a dramatic improvement in drug permeation across epithelial tissue. In addition, a formulation containing PYY(3-36) and TJM peptide was dosed intranasally in rabbits, resulting in a dramatic increase in bioavailability. The TJM peptide was as or more effective in enhancing PYY(3-36) permeation in vivo at a 1000-fold lower molar concentration compared to using LMW enhancers. Based on these in vitro and in vivo data, the novel TJM peptide represents a promising advancement in intranasal formulation development.
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PMID:Therapeutic utility of a novel tight junction modulating peptide for enhancing intranasal drug delivery. 1662 59


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