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 expression of nerve growth factor receptor (NGFR) transcripts was investigated with in situ hybridization techniques in the CNS of chick embryos from 3 days of incubation (E3) to 14 days posthatch (P14). The time course and distribution of NGFR expression was compared with the development of the cholinergic phenotype. Cholinergic properties were assessed by immunolabeling for choline acetyltransferase (ChAT) and histochemistry for acetylcholinesterase (AchE) activity. NGFR transcripts are expressed transiently in the inner plexiform layer and ganglion cell layer of the retina (E4-P1), neostriatum and hippocampus (E18), infundibular hypothalamus (E7-18), spiriform complex (E9-15), layers 2, 3 (E9-18), and 10 (E11-18) of the optic tectum, nucleus mesencephalicus profundus, pars ventralis (E9-18), parvicellular isthmic nucleus (E7-P1), magnocellular isthmic nucleus (E9-E18), nucleus semilunaris (E7-18), isthmo-optic nucleus (E7-P14), rostral motor nuclei (E5-18), developing cerebellum (E7-15), internal granule cell layer (E11-18) and Purkinje cell layer (E15-P14) of the cerebellar cortex, and the inferior olivary nucleus (E9-15). A small number of neuronal populations with embryonic expression of NGFR remain strongly NGFR-positive in the posthatch animal:habenular nuclei (labeled after E5), nucleus subrotundus (after E9), mesencephalic trigeminal nucleus (after E5), caudal parts of locus ceruleus and nucleus subceruleus (after E7), medullar reticular nuclei (after E11), and motor nuclei IX, X, and XII (after E9). The majority of neuronal populations with NGFR expression show cholinergic properties in development, and NGFR expression always precedes the onset of ChAT immunoreactivity. Postnatal expression of growth factor receptors is largely confined to neurons of the reticular type. NGFR expression in avian CNS nuclei differs from that in mammals. Early loss of NGFR expression in the cholinergic basal forebrain (which remains strongly NGFR positive in mammals) and persistent NGFR expression in parts of the avian locus ceruleus indicate changes of growth factor receptor expression and growth factor requirements in phylogeny. Knowledge of the time and distribution of NGFR expression in the chick embryo will facilitate the assessment of specific functions of NGF and NGF-like molecules in an embryonic model with easy access for experimental manipulations.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Expression of nerve growth factor (NGF) receptors in the brain and retina of chick embryos: comparison with cholinergic development. 165 88

The aim of this study was to examine the development of the basalocortical pathway by using choline acetyltransferase and nerve growth factor receptor immunocytochemistry, acetylcholinesterase histochemistry and retrograde axonal transport. The observations were made in the ferret because in this species brain development occurs over a much more protracted period than in the rat. Staining for choline acetyltransferase immunoreactivity in the brain was minimal before birth. Adult levels of staining for the enzyme were not seen in cell bodies until three weeks after birth and in axons up to six weeks after birth. This, however, did not mean that presumptive cholinergic pathways are absent early in development. There was strong staining for nerve growth factor receptor in basal forebrain neurons from at least two weeks before birth. Positive staining for acetylcholinesterase was found in axons that begin to invade the cerebral cortex a week before birth. The retrograde axonal transport technique showed that the basalocortical pathway has a normal organization in the neonate. The conclusion is that cholinergic pathways form early in the prenatal period in the ferret but express their transmitter function late in postnatal development.
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PMID:Early development of the nucleus basalis-cortical projection but late expression of its cholinergic function. 168 50

Different doses of the excitotoxin quisqualate were used to make lesions in the caudal part of the ferret nucleus basalis, i.e. the part that projects to the visual cortex. The higher doses of the excitotoxin destroyed all nerve growth factor receptor-immunoreactive cells in the caudal nucleus basalis and gave rise to up to 75% loss of acetylcholinesterase-containing axons in the visual cortex. In sections stained for Nissl substance there was generalized tissue damage around the injection sites and extensive loss of all neuron types in areas surrounding the caudal nucleus basalis. Lower doses of the excitotoxin damaged only a proportion of the nerve growth factor receptor-immunoreactive neurons in the caudal nucleus basalis and produced a much lower depletion of acetylcholinesterase-positive fibres in the visual cortex. The only damage seen in sections stained for Nissl substance was a loss of magnocellular neurons in the vicinity of the injection sites. A quantitative morphological approach was used to show that either one week or three months after the lesions there was a linear correlation between the proportion of acetylcholinesterase-positive axons lost in the visual cortex and the proportion of nerve growth factor receptor-immunoreactive cells that had disappeared from the caudal nucleus basalis. Since the correlation lines for the short-term (one week) survival and the long-term (three months) survival experiments coincided, this indicated that no collateral sprouting of cholinergic axons had occurred in the visual cortex of the long-term survival animals regardless of size of the lesion in the nucleus basalis.
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PMID:Sprouting of cholinergic axons does not occur in the cerebral cortex after nucleus basalis lesions. 172 89

The compound 2,5-hexanedione (HD) produces axonopathies in peripheral nerves characterized by selective accumulation of neurofilaments. Its direct actions on neurotransmitter-specific neurons in the brain are unknown. In an attempt to address this latter issue, we infused HD into the fimbria and evaluated histochemically and immunohistochemically possible structural alterations in cholinergic neurons projecting from the basal nuclear complex to the hippocampus. Putative cholinergic fibers expressing nerve growth factor receptor and acetylcholinesterase showed increases in caliber and perturbations in trajectories 2-4 days following HD treatment. Similar morphologic changes were observed in neuronal elements processed for the 68 kDa neurofilament protein. At 7 days, short collateral ramifications appeared in many cholinergic axons that were suggestive of neurite outgrowth. Correlated with these fiber alterations was a transient reduction in the number of medial septal and diagonal band somata expressing choline acetyltransferase, which returned to control levels within 6 weeks following HD treatment. These data support the view that neurofilaments play an important, perhaps cytoarchitecturally stabilizing, role in regulating axonal morphology in certain populations of cholinergic neurons.
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PMID:Cholinergic fiber perturbations and neuritic outgrowth produced by intrafimbrial infusion of the neurofilament-disrupting agent 2,5-hexanedione. 184 77

The microtubule disrupting agent, colchicine, was infused both bilaterally and unilaterally into the fimbria of the rat brain. Such infusions produced a transient impairment in radial-arm maze performance during the first week following surgery but only in bilaterally injected animals. This behavioral finding was correlated with a reduction in the number of neurons expressing choline acetyltransferase and nerve growth factor receptor in the septum and vertical limb of the diagonal band but not in other regions of the basal nuclear complex. The altered expression of the two neurochemical markers was not due to cellular degeneration because numbers of neurons demonstrated by Nissl staining were unchanged. Putative cholinergic fibers in the fimbria demonstrating acetylcholinesterase and nerve growth factor receptor also showed aberrations in caliber, shape, and course.
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PMID:Intrafimbrial colchicine produces transient impairment of radial-arm maze performance correlated with morphologic abnormalities of septohippocampal neurons expressing cholinergic markers and nerve growth factor receptor. 216 23

Normal aged human basal forebrain tissue immunohistochemically stained with a monoclonal antibody for nerve growth factor receptor (NGFR) revealed a continuum of NGFR containing neurons in brain regions corresponding to Ch1-Ch4. NGFR immunoreactive neurons were observed within the medial septum (Ch1), vertical (Ch2) and horizontal (Ch3) limb nuclei of the diagonal band and nucleus basalis (Ch4) complex. Occasional dystrophic NGFR containing neurons were observed within the Ch subfields. Colocalization experiments demonstrated that virtually all (95%) NGFR containing perikarya stained positively for the specific cholinergic marker acetylcholinesterase. On the other hand, occasional cholinergic negative NGFR positive neurons were seen in the putamen of the striatal complex. In Alzheimer's disease, subfields of the basal forebrain revealed extensive neuronal loss and shrinkage, dystrophic fibers as well as normal appearing neurons. Each AD case exhibited an individual pattern of cell loss. Within the Ch1-4 subfields NGFR and ChAT colocalized, indicating that the NGFR remained coupled to cholinergic neurons in AD. In some Parkinson's cases there was a severe loss of NGFR containing basal forebrain neurons. These findings indicate that NGFR containing basal forebrain neurons colocalize with ChAT, are severely affected in AD, in some PD cases, and NGFR remains coupled to cholinergic perikarya in both neurodegenerative disorders.
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PMID:Nerve growth factor receptor expressing human basal forebrain neurons: pathologic alterations in Alzheimer's and Parkinson's disease. 255 38

Previous work has indicated that nerve growth factor specifically and selectively increases choline acetyltransferase and acetylcholinesterase in organotypic cultures of rat basal forebrain-medial septal area. To determine whether these actions are potentially receptor-mediated, organotypic and dissociated basal forebrain-medial septal area cultures were examined. Two independent methods, [125I]nerve growth factor binding and immunocytochemistry with a monoclonal nerve growth factor receptor antibody (192-IgG), detected specific receptors. The nerve growth factor receptors were localized to two different cellular populations: flat, large, non-neuron-like cells, and small, round, process-bearing, neuron-like cells. Dissociation studies with [125I]nerve growth factor suggested that high-affinity receptors were localized to the neuron-like population, while only low-affinity receptors were localized to the non-neuron-like cells. We tentatively conclude that nerve growth factor may elicit cholinergic effects by directly binding to high-affinity receptors on neurons. To begin examining receptor regulation, cultures were exposed to exogenous, unlabeled nerve growth factor continuously for 10 days before binding studies were performed. Prior exposure to nerve growth factor did not alter binding characteristics of the receptor, using the present methods.
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PMID:Localization of high-affinity and low-affinity nerve growth factor receptors in cultured rat basal forebrain. 284 89

PC12 cells, which differentiate morphologically and biochemically into sympathetic neuron-like cells when treated with nerve growth factor, also respond to fibroblast growth factor. Some of the changes induced by fibroblast growth factor are similar to those seen after nerve growth factor treatment. Specifically, pituitary fibroblast growth factor causes the formation of processes initially comparable to those produced by nerve growth factor. However, in contrast to the outgrowth induced by nerve growth factor, which continues for several days, the outgrowth of processes induced by fibroblast growth factor ceases after about 3 days, even though fresh fibroblast growth factor is added. After about 6 days the processes induced by fibroblast growth factor have virtually disappeared. In this regard the processes induced by fibroblast growth factor are very similar to those induced by dibutyryl cyclic adenosine 3':5'-monophosphate (dBcAMP). The addition of nerve growth factor and fibroblast growth factor together appears to produce a synergistic effect on process formation, as does the simultaneous addition of nerve growth factor and dBcAMP. Cells pretreated (or primed) with nerve growth factor are able to regenerate processes much more rapidly in the presence of nerve growth factor than cells which have not been pretreated. When fibroblast growth factor is added to cells primed with nerve growth factor, more rapid regeneration of processes also occurs. The regeneration of neurites in response to either factor is blocked by the addition of an inhibitor of methylation. The process formation induced by fibroblast growth factor is preceded, as is the outgrowth in response to nerve growth factor treatment, by an induction of ornithine decarboxylase, a decrease in the phosphorylation of a specific cytoplasmic protein, and an increase in the phosphorylation of a specific non-histone nuclear protein. The effects of fibroblast growth factor and of nerve growth factor on ornithine decarboxylase are additive. Fibroblast growth factor does not cause an increase in the activity of acetylcholinesterase; nerve growth factor does. Fibroblast growth factor does not appear to be acting through the nerve growth factor receptor. The binding of iodinated nerve growth factor to PC12 cells is specific and is not inhibited by the presence of fibroblast growth factor. In addition, anti-nerve growth factor serum does not interfere with the action of fibroblast growth factor.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:The effect of fibroblast growth factor on PC12 cells. 298 39

Neurotrophins and neural cytokines are two broad classes of neurotrophic factors. It has been reported that ciliary neurotrophic factor (CNTF) and brain-derived neurotrophic factor (BDNF) prevent the degeneration of axotomized neonatal motor neurons. In addition, BDNF is transported retrogradely to alpha-motor neurons following injection into the muscle, and patterns of BDNF expressed in spinal cord and muscle suggest a physiological role for this factor in motor neurons. In the present study, we characterize the effects of BDNF on axotomized neonatal facial motor neurons and extend these observations to adult models of motor neuron injury (axotomy-induced phenotypic injury of lumbar motor neurons). BDNF reduces axotomy-induced degeneration of neonatal neurons by 55% as determined by Nissl staining (percentage of surviving neurons in vehicle-treated cases, 25%; in BDNF-treated cases, 80%). Rescued neurons have an intact organelle structure but appear smaller and slightly chromatolytic on electron microscopic analysis. As demonstrated by intense retrograde labeling with horseradish peroxidase (HRP) applied to the proximal stump of the facial nerve, neurons rescued by BDNF have intact mechanisms of fast axonal transport. CNTF did not appear to have significant effects on neonatal motor neurons, but the lack of efficacy of this factor may be caused by its rapid degradation at the application site. BDNF is not capable of reversing the axotomy-induced reduction in transmitter markers [i.e., the acetylcholine-synthesizing enzyme choline acetyltransferase (ChAT) or the degrading enzyme acetylcholinesterase (AChE) in neonatal or adult animals or the axotomy-induced up-regulation of the low-affinity neurotrophin receptor p75NGFR (nerve growth factor receptor) in adult motor neurons. However, BDNF appears to promote the expression of p75NGFR in injured neonatal motor neurons. In concert, the findings of the present study suggest that BDNF can significantly prevent cell death in injured motor neurons. However, this neurotrophin may not be a retrograde signal associated with the induction and/or maintenance of some mature features of motor neurons, particularly their transmitter phenotype.
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PMID:Further characterization of the effects of brain-derived neurotrophic factor and ciliary neurotrophic factor on axotomized neonatal and adult mammalian motor neurons. 751 7

The authors studied rectal suction biopsy material in 60 consecutively treated patients suspected of having Hirschsprung's disease (HD) (age range, 3 days to 12 years). According to acetylcholinesterase (AChE) staining, 10 patients had HD, three had neuronal intestinal dysplasia (NID), and 47 were normal. The diagnoses were confirmed by H&E staining of biopsy material and by examination of surgically resected material in the HD and NID cases. The 60 cases were stained with a monoclonal antibody to the nerve growth factor receptor (NGFR) using immunohistochemistry on fresh frozen biopsy tissue. In the 47 normal biopsy specimens, there was a large number of immunoreactive fibers in the lamina propria, and staining of the muscularis mucosae and submucous ganglia. In contrast, there were no immunoreactive fibers in the lamina propria in patients with HD and NID. A striking finding was the strong expression of immunoreactivity on the perineurium of submucosal hypertrophic nerve trunks in cases of HD. The results indicate that NGFR immunoreactivity is similar in specificity and sensitivity to AChE in the diagnosis of HD. Because the technique uses an immunocytochemical rather than a histochemical technique and the results were easier to interpret, NGFR staining may be an important additional technique to diagnose HD.
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PMID:Nerve growth factor receptor staining of suction biopsies in the diagnosis of Hirschsprung's disease. 780 51


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