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:3.1.1.8 (cholinesterase)
12,691 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In the normal dog we have found that cholinesterase and tyrosine hydroxylase (TH) histochemistry define a mosaic structure of the caudate nucleus that is similar to that described in other species. To determine if nigrostriatal afferents interlocked with this mosaic we injected dogs with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), a toxin specific to dopaminergic nigrostriatal cells. Alternate sections in the caudate nucleus stained for acetylcholinesterase, TH, and terminal degeneration revealed that the areas of densest degeneration were localized to the matrix, thereby outlining areas of much lighter degeneration which were coincident with the patches. This pattern of terminal degeneration suggests the existence of subcomponents of the dopaminergic nigrostriatal pathway, at least one of which might be selectively vulnerable to MPTP.
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PMID:MPTP produces a pattern of nigrostriatal degeneration which coincides with the mosaic organization of the caudate nucleus. 290 3

Rats were treated for 2-6 weeks with guanethidine after which their superior cervical ganglia were removed. Ganglionic tyrosine hydroxylase and alpha-bungarotoxin binding sites were reduced by the guanethidine treatment indicating adrenergic cell body destruction. Choline acetyltransferase activity and acetylcholine content of ganglia were not clearly changed by the guanethidine treatment, indicating that the drug does not destroy presynaptic terminals and that these presynaptic indicators do not adapt markedly to postsynaptic loss. The cholinesterase in the ganglia was reduced by guanethidine treatment, but such ganglia retained their ability to accumulate surplus acetylcholine when they were incubated with physostigmine. This is interpreted as indicating surplus acetylcholine accumulation is a presynaptic phenomenon. Choline uptake by resting ganglia was not reduced as a result of guanethidine treatment nor was it affected by preganglionic denervation. This is interpreted as indicating that during rest, choline uptake is into supporting cells or intraganglionic cells rather than cholinergic nerve terminals or adrenergic cell bodies.
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PMID:Effect of chemical destruction of adrenergic neurones on some cholinergic mechanisms in adult rat sympathetic ganglia. 614 15

In order to delineate the type and distribution of autonomic nerves within the atrial and ventricular myocardium of the neonatal human heart, numerous samples of atrial and ventricular myocardium from 4 neonatal human hearts with no cardiac anomaly, freshly obtained at necropsy, were processed and studied using immunohistochemical and enzyme histochemical techniques. The antisera included those used to demonstrate protein gene product (PGP) 9.5 as a general neural marker, dopamine beta-hydroxylase (DBH) and tyrosine hydroxylase (TH) as indicators for presumptive sympathetic neural tissue, and neuropeptide Y (NPY). A histochemical technique was used to reveal tissue cholinesterase activity. Numerous PGP-immunoreactive (PGP-IR) nerves were seen in the atrial myocardium, forming perivascular plexuses and lying in close apposition to myocardial cells. Fewer PGP-IR nerves were found amongst the myocardium of the ventricles. Both DBH-IR and TH-IR nerves demonstrated a similar pattern of distribution as that of PGP-IR nerves; in the atria, however, they were less numerous, while in the ventricles, their density approximated to that of PGP-IR nerves. Relatively few NPY-IR nerves were observed either in the atrial or the ventricular myocardium. The density of acetylcholinesterase (AChE) positive nerves in the walls of the atria was less than that of PGP-IR nerves although their distribution patterns were similar. In the ventricles, AChE positive nerves were rarely observed. It is concluded that the neonatal human heart possesses a rich supply of autonomic nerves. The atria possess at least two populations of nerves, presumably sympathetic and vagal, whereas the walls of the ventricles are innervated principally by presumptive sympathetic nerves.
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PMID:The innervation of the human myocardium at birth. 759 71

Islets transplanted beneath the kidney capsule become reinnervated during the first 3-4 months after implantation by both afferent and efferent nerve fibers. To evaluate the importance of the implantation organ for this process, the present study compared both the degree and the types of nerve fibers reinnervating islets transplanted into the liver, kidney, and spleen. For this purpose, 150 syngeneic islets were grafted under the kidney capsule of C57BL/6 mice. In addition, the same animals were injected with 150 islets into the spleen or liver. All animals were killed 14 weeks after transplantation, after which the graft-bearing organs were processed for indirect immunofluorescence for neuropeptides and tyrosine hydroxylase (TH), and with acetyl cholinesterase (AchE) staining to visualize nerve fibers. Both afferent (containing substance P and/or calcitonin gene-related peptide) and parasympathetic (containing vasoactive intestinal peptide or AchE) nerve fibers were absent from islets implanted into the spleen; an occasional CGRP fiber was seen in islets implanted into the liver; and all these fibers were regularly seen in islets implanted beneath the renal capsule. The islets implanted into the liver or spleen contained a dense network of sympathetic (containing neuropeptide Y and TH) nerve fibers that was often more dense than in the islet grafts under the kidney capsule. One-fifth of islets implanted into the liver were, however, completely devoid of demonstrable nerve fibers. In conclusion, there are marked differences with regard to the pattern of reinnervation of islets transplanted to different implantation sites.
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PMID:Reinnervation of transplanted pancreatic islets. A comparison among islets implanted into the kidney, spleen, and liver. 768 93

Administration of the irreversible cholinesterase inhibitor isoflurophate (diisopropylfluorophosphate, DFP) before 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) enhanced the loss in tyrosine hydroxylase activity and dopamine and 3,4-dihydroxy-phenylacetic acid content in the striatum of mice in a dose-dependent manner. The effect of DFP on the MPTP-induced changes of dopaminergic markers was evident 30 days after initiating treatment, suggesting augmented neurotoxicity. Neurotoxicity was also enhanced by prior treatment with nicotine, carbachol or oxotremorine. We conclude that activation of either muscarinic or nicotinic receptors enhances the neurotoxicity of MPTP.
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PMID:Enhanced MPTP neurotoxicity after treatment with isoflurophate or cholinergic agonists. 791 17

Heart rate is regulated by the autonomic nervous system but little is known about the pattern of innervation of the pacemaker in the sinoatrial node, or the subpopulations of nerves involved. Therefore in this study the pacemaker was located using electrophysiological methods and the pattern of innervation established by cholinesterase staining. In subsequent experiments, subpopulations of sympathetic, sensory and parasympathetic nerves were identified. Sympathetic nerves were labelled by glyoxylic acid-induced catecholamine fluorescence or an antiserum raised against tyrosine hydroxylase (TH). These experiments showed that the entire sinoatrial node was densely innervated by sympathetic axons, the majority of which were immunoreactive for neuropeptide Y (NPY). There were a few axons which were only immunoreactive for TH. Sensory nerves which were immunoreactive for both substance P (SP) and calcitonin gene-related peptide (CGRP) were also found throughout the sinoatrial node. In the absence of a selective marker for parasympathetic neurons, hearts were extrinsically denervated by placing them in organotypic culture to allow degeneration of extrinsic axons. In this way intrinsic parasympathetic neurons could be characterised. These experiments revealed several distinct populations of parasympathetic nerves which innervated only a small, discrete part of the sinoatrial node. These populations were immunoreactive for NPY, somatostatin (SOM) or vasoactive intestinal peptide (VIP) alone, or SOM combined with NPY, SOM with dynorphin B, and SOM with SP. These results highlight a remarkable difference in the pattern of innervation of the sinoatrial node by the sympathetic and parasympathetic nervous systems. Furthermore the presence of several distinct populations of autonomic cardiac neurons indicates a further complexity in neuronal regulation of heart rate.
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PMID:Innervation of the pacemaker in guinea-pig sinoatrial node. 801 78

To determine if systemically administered antibodies could reach antigenic targets and cause immunologic lesions in brains of newborn rats, murine monoclonal antibodies against rat acetylcholinesterase were injected i.p. on the first postnatal day. As early as 24 h after injection, antibodies were detected immunocytochemically in brain parenchyma, along with punctate debris that showed intense cholinesterase activity. Total acetylcholinesterase activity in the brain dropped by 30%, and 10S activity was almost undetectable at day 3, implying true enzyme loss since the antibodies did not directly impair catalytic function. At day 7, 10S acetylcholinesterase began to recover but the activity remained only half that of controls. At day 12, total acetylcholinesterase activity was still reduced (30% in whole brain, 40% in cerebral cortex), consistent with lasting damage to cholinesterase-expressing cortical neurons. This conclusion was confirmed by histochemical experiments showing a nearly complete disappearance of acetylcholinesterase fiber-staining in cerebral cortex and basal ganglia at days 4 and 8, with residual deficits at day 12. Choline acetyltransferase activity decreased in the cerebral cortex, implying a loss of cholinergic terminals, but specifically immunoreactive perikarya remained abundant in the basal forebrain. Immunocytochemistry showed no obvious changes in three non-cholinergic markers: tyrosine hydroxylase, tryptophan hydroxylase, and glutamic acid decarboxylase. Overall, it appeared that acetylcholinesterase antibodies induced widespread but reversible damage of cholinergic fibers and terminals, while sparing cholinergic cell bodies and many other neural systems.
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PMID:Lesion of central cholinergic systems by systemically administered acetylcholinesterase antibodies in newborn rats. 851 43

In this paper we study the septal complex architecture in the lizard Podarcis hispanica (Lacertidae). Histochemical and immunohistochemical techniques were used to define the distribution of zinc (Timm stain), acetyl cholinesterase (AChase), gamma-aminobutyric acid (GABA), tyrosine hydroxylase (TH), dopamine (DA), serotonin (5-HT), and two neuropeptides: leu-enkephalin (L-ENK) and substance P (SP). These reactions delineate a coherent map of nine septal nuclei that are named with a topographical nomenclature: anterior, lateral, ventromedial, medial, dorsolateral, ventrolateral, and dorsal septal nuclei, nucleus septalis impar, and nucleus of the posterior pallial commissure. The anterior septal nucleus is characterized by intense reaction for zinc and the presence of fibers immunoreactive for GABA, 5-HT, and L-ENK, which form pericellular nests. The lateral septal nucelus shows intense reaction for zinc, a high density of GABA-immunoreactive cells, and L-ENK-immunoreactive fibers forming basketlike figures around unstained somata. The ventromedial septal nucleus shows intense AChase reactivity, a dense network of 5-HT-immunoreactive fibers, and virtually no labeling for the other histochemical stains. The medial septal nucleus is defined by heavy reactivity for zinc, dense DA/TH and L-ENK innervations, and the presence of L-ENK-immunoreactive cells. The dorsolateral septal nucleus shows intense AChase staining in the neuropile and a dense network of fibers immunoreactive for 5-HT and DA/TH, but it shows low staining for zinc. The ventrolateral septal nucleus shows L-ENK-immunoreactive cells and a dense L-ENK innervation, but low reactivity for zinc. The dorsal septal nucleus, intermingled with the fimbrial fibers, shows a dense population of GABA-immunoreactive cells and terminals, but it is unreactive for zinc. Two subdivisions can be established in this dorsal septal nucleus: the dorsal part, intensely reactive for AChase and innervated by 5-HT fibers, and the central part, which shows L-ENK-immunoreactive neurons and fibers without reactivity for either AChase or 5-HT. The nucleus septalis impar, traversed by the fibers of the anterior pallial commissure (mildly reactive for zinc), shows reaction for AChase but low (if present) reactivity for the remaining markers. The nucleus of the posterior pallial commissure shows a generally low reactivity for the histochemical reactions employed. The distribution of these markers is similar to that found in other squamate reptiles and allows for a direct comparison with the septal formation of mammals. Such a comparison reinforces the view that the limbic system has undergone a conservative evolution within vertebrates.
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PMID:The septal complex of the telencephalon of the lizard Podarcis hispanica. I. Chemoarchitectonical organization. 855 41

Mechanisms of relaxation induced by nerve stimulation were examined in isolated porcine iris sphincter muscle in reference to norepinephrine, nitric oxide (NO) and vasoactive intestinal polypeptide (VIP) and the functional interaction of inhibitory and excitatory nerves. Changes in isometric tension were recorded in strips of the sphincter pupillae, which were stimulated by transmurally applied electrical pulses. The presence of neurons containing acetylcholinesterase and tyrosine hydroxylase (TH) was determined histochemically. Transmural electrical stimulation (0.5-20 Hz) produced a frequency-related contraction, which was reversed to a relaxation by atropine in prostaglandin F2alpha-contracted strips. The relaxant response was abolished by timolol and suppressed by metoprolol, a beta1-adrenoceptor antagonist, but was not influenced by butoxamine, a beta2-receptor antagonist. Norepinephrine-induced relaxations were also attenuated only by timolol and metoprolol. Treatment with NG-nitro-L-arginine, a NO synthase inhibitor, and [D-p-Cl-Phe6,Leu17]VIP, a VIP receptor antagonist, did not inhibit the neurogenic relaxation. Contractions induced by nerve stimulation were potentiated by timolol and physostigmine but not by the NO synthase inhibitor. In the sphincter muscle, cholinesterase- and TH-positive nerve fibers and bundles were histologically detected. It is concluded that porcine iris sphincter is innervated by cholinergic excitatory and adrenergic inhibitory nerves. The neurogenic relaxation is associated solely with activation of beta1 adrenoceptors by norepinephrine but is not mediated by NO or VIP.
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PMID:Mechanisms underlying the neurogenic relaxation of isolated porcine sphincter pupillae. 1019 8

In order to study the changes in the pattern of autonomic innervation of the human cardiac conduction system in relation to age, the innervation of the conduction system of 24 human hearts (the age of the individuals ranged from newborn to 80 years), freshly obtained at autopsy, was evaluated by a combination of immunofluorescence and histochemical techniques. The pattern of distribution and density of nerves exhibiting immunoreactivity against protein gene product 9.5 (PGP), a general neural marker, dopamine beta-hydroxylase (DBH) and tyrosine hydroxylase (TH), indicators for presumptive sympathetic neural tissue, and those demonstrating positive acetylcholinesterase (AChE) activity, were studied. All these nerves showed a similar pattern of distribution and developmental changes. The density of innervation, assessed semiquantitatively, was highest in the sinus node, and exhibited a decreasing gradient through the atrioventricular node, penetrating and branching bundle, to the bundle branches. Other than a paucity of those showing AChE activity, nerves were present in substantial quantities in infancy. They then increased in density to a maximum in childhood, at which time the adult pattern was achieved and then gradually decreased in density in the elders to a level similar to or slightly less than that in infancy. In contrast, only scattered AChE-positive nerves were found in the sinus and atrioventricular nodes, but were absent from the bundle branches of the infant heart, whereas these conduction tissues themselves possessing a substantial amount of pseudocholinesterase. During maturation into adulthood, however, the conduction tissues gradually lost their content of pseudocholinesterase but acquired a rich supply of AChE-positive nerves, comparable in density to those of DBH and TH nerves. The decline in density of AChE-positive nerves in the conduction tissues in the elders was also similar to those of DBH and TH nerves. Our findings of initial sympathetic dominance in the neural supply to the human cardiac conduction system in infancy, and its gradual transition into a sympathetic and parasympathetic codominance in adulthood, correlate well with the physiologic alterations known to occur in cardiac rate during postnatal development. The finding of reduction in density of innervation of the conduction tissue with ageing is also in agreement with clinical and electrophysiological findings such as age-associated reduction in cardiac response to parasympathetic stimulation. Finally, our findings also support the hypothesis that, in addition to the para-arterial route, the parafascicular route of extension along the conduction tissue constitutes another pathway for the innervation of the conduction system of the human heart during development.
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PMID:Autonomic innervation of the human cardiac conduction system: changes from infancy to senility--an immunohistochemical and histochemical analysis. 1159 May 94


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