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)

1. A number of observations, as listed below, suggested a cholinergic basis for inhibitory interactions between photoreceptors of the eye in the nudibranch mollusk Hermissenda crassicornis. 2. The isolated eyes synthesized and accumulated acetylcholine but not other putative neurotransmitter substances. Synthesis and accumulation were determined by electrophoretic separation of products that incorporated radioactive label. Electron microscopic visualization of clear round vesicles within the photoreceptors' somata and axon hillocks was consistent with synthesis and storage of acetylcholine within these cells. 3. Pharmacologic experiments indicated the presence of cholinergic receptors on the terminal branches of the photoreceptors, which are pre- and postsynaptic to each other. Carbachol or nicotine produced hyperpolarization of the photoreceptors' membrane accompanied by a reduction of the input resistance. The reversal potential of carbachol-induced hyperpolarization coincided with the reversal potentials of the IPSPs that followed, one for one, impulses of neighboring photoreceptors. Eserine often caused blockade of the IPSPs. This blockade was associated with substantial membrane hyperpolarization and reduction of membrane resistance. 4. Neuronal endings within the optic tract in the area of the photoreceptor's terminal branches stained for acetylcholinesterase. 5. The results of these different experiments, especially when considered together, strongly suggest, although by no means unequivocally demonstrate, that the neurotransmitter of the photoreceptors is acetylcholine.
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PMID:Cholinergic features of photoreceptor synapses in Hermissenda. 3 73

Neuronal membranes of postsynaptic origin twofold enriched in acetylcholinesterase, muscarinic acetylcholinereceptor and (Na+/K+)-ATP-Phosphohydrolase, proteins associated with cholinergic nerve excitability, were prepared with yields between 60 and 75% from bovine caudate nucleus. On subfractionation of these membranes an additional twofold enrichment of the mentioned proteins is achieved in different subfractions. SDS-gradient gel electrophoresis shows that these subfractions have slightly different polypeptide compositions. Neuronal membranes of presynaptic origin on the other hand, prepared from purified synaptosomes, possess only small amounts of the mentioned proteins, showing no enrichment with respect to the homogenate. Solubilization of acetylcholinesterase with 1 M NaC1 as well as of muscarinic acetylcholinreceptor with 2 M NaC1 does not succeed. These proteins are therefore not solely bound by ionic forces to the isolated membranes from bovine caudate nucleus.
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PMID:[Attempts to enrich and to solubilize the muscarinic acetylcholinereceptor from bovine caudate nucleus (author's transl)]. 22 Aug 10

A case of adynamic bowel syndrome is described. Full thickness biopsies of the large bowel showed the presence of ganglion cells, no acetylcholinesterase positive nerves in the lamina propria, submucosa or among the smooth muscle cells of the circular and longitudinal muscle coats, and absence of the argyrophil plexus. Electron microscopic examination showed replacement of the normal axon bundle by vacuolated tracts with small round bodies in one area--probably viral. Neuronal cytoplasm also showed similar vacuolation. It is suggested that the damage to the cholinergic innervation may be caused by a neurotoxic agent.
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PMID:Adynamic bowel syndrome. Report of a case with disturbance of the cholinergic innervation. 60 97

Medial hypothalamic tissue of 1 to 4 days old rats was dissociated and cultured in vitro for 8--10 days. Neuronal perikarya were demonstrated by supravital methylene blue staining and electron microscopy. Synapses with typical vesicles and subsynaptic thickening were also observed. 3H-GABA was taken up into a small percentage of the cells in the cultures. Neuron-like perikarya and long processes accumulated the label while many neurons contained much less activity. Some astroglial and oligodendroglial cells and processes also accumulated GABA. A few neurons in these cultures contained acetylcholinesterase. It is concluded that neurons concentrating GABA and containing acetylcholinesterase are present in the hypothalamus of rats of 1 to 4 days of age and can be maintained in dissociated cell culture.
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PMID:3H-GABA uptake and acetylcholinesterase activity in dissociated cell cultures of the medial hypothalamus. 103

The locus coerulus is a densely packed group of neurons in the floor of the fourth ventricle, and is the largest aggregate of noradrenaline-containing cells in the mammalian brain. The distribution within the locus of acetylcholinesterase (AChE), which is present in high concentration, has been studied at light and electron microscope level, both in normal rats and in ones treated with 6-hydroxydopamine. Neuronal enzyme activity is entirely intracellular and mainly concentrated in stacks of ER which occupy much of the cell cytoplasm. There are no indications of a cholinergic input. After 6-hydroxydopamine treatment extensive cell death occurs and AChE activity virtually disappears. A majority of the many blood vessels in the locus also stain strongly for AChE, unlike those present in most other areas of the rat brain. The locus coeruleus therefore represents an area of the rat brain with a high content of AChE, but no evidence of a cholinergic mechanism. Some possible explanations for this anomalous presence of AChE are briefly discussed.
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PMID:The localization of acetylcholinesterase in the locus coeruleus of the normal rat and after 6-hydroxydopamine treatment. 120 68

Recent evidence suggests that termination of cholinergic transmission is just one of the many ways in which acetylcholinesterase (AChE) could influence neuronal function. Neuronal AChE can be secreted from several brain regions, while purified AChE possesses several properties (in addition to its cholinesterase activity) that can affect neuronal function, including the abilities to influence certain membrane conductances, enhance excitatory amino acid transmission and hydrolyse peptides. Loss of AChE and its non-classical actions would have a profound effect on brain function in neurodegenerative diseases such as Alzheimer's disease where there is widespread loss of AChE-containing neurons.
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PMID:Secreted acetylcholinesterase: non-classical aspects of a classical enzyme. 128 48

Neuronal cells from cerebral hemispheres of 14-day-old rats were grown for 6 days in a serum-free, chemically defined medium. About 95-98 and 3% of these cells were neurofilament and acetylcholinesterase (AChE)-positive, respectively. The addition of basic fibroblast growth factor (bFGF) at three developmental stages, i.e. at 4 h, 2 and 4 days resulted in an increase (about 2-fold) of the number of AChE-positive neurons. The enzyme reaction was present in the cell body as well as in the fibers, which often ramified extensively under the influence of bFGF. Treatment with bFGF after the 2nd day of culture had no or only a low stimulatory effect. Our findings indicate that bFGF affects the development of AChE-containing neurons, i.e. cholinoceptive neurons from rat cerebrum.
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PMID:Influence of basic fibroblast growth factor on the development of cholinoceptive neurons from fetal rat cerebrum in culture. 129 49

The involvement of the NMDA receptor in the neurotoxicity induced by soman, an organophosphorus compound which irreversibly inhibits cholinesterase, was studied in guinea pigs. The drug MK-801 (0.5, 1 or 5 mg/kg, i.p.) was given as a pretreatment before a convulsant dose of soman or as a posttreatment (30, 100 or 300 micrograms/kg, i.m.) 5 min after the development of soman-induced status epilepticus. Pyridostigmine, atropine and pralidoxime chloride were also given to each subject to counteract the lethality of soman. All subjects that were challenged with soman and given the vehicle for MK-801 (saline) exhibited severe convulsions and electrographic seizure activity. Neuronal necrosis was found in the hippocampus, amygdala, thalamus and the pyriform and cerebral cortices of those subjects surviving for 48 hr. Pretreatment with 0.5 or 1 mg/kg doses of MK-801 did not prevent nor delay the onset of seizure activity but did diminish its intensity and led to its early arrest. At the largest dose (5 mg/kg), MK-801 completely prevented the development of seizure activity and brain damage. Posttreatment with MK-801 prevented, arrested or reduced seizure activity, convulsions and neuronal necrosis in a dose-dependent manner. The NMDA receptor may play a more critical role in the spread and maintenance, rather than the initiation of cholinergically-induced seizure activity.
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PMID:Dizocilpine (MK-801) arrests status epilepticus and prevents brain damage induced by soman. 152 53

A primary culture system of nearly pure neuronal cells from 14-day-old fetal rat spinal cord has been developed by combining a preplating step, the use of a chemically defined serum-free medium, and borated polylysine-coated dishes that prevented the formation of cell aggregates. About 98% of the cells were found to be immunostained with neuron-specific enolase antibodies, confirming their neuronal nature. The cultures are composed essentially of a population of non-motoneurons and contain few motoneurons, characterized by their large size and multipolar aspect, the presence of acetylcholinesterase (AChE), and the intense immunoreaction for growth-associated protein GAP-43. Neuronal precursor cells are also present in these cultures and proliferate during the first 3 days. The addition of bovine brain basic fibroblast growth factor (bFGF) stimulates their proliferation over a period of 2 days, as determined by measurement of [125I]iododeoxyuridine incorporation and by immunocytochemical reaction after bromodeoxyuridine incorporation into nuclei. The proliferating cells were characterized as neurons by immunostaining against neuron-specific enolase. Recombinant human bFGF and bovine brain acidic FGF (aFGF) exerted similar effects. Other growth factors, including epidermal growth factor (EGF), transforming growth factor beta 1 (TGF-beta 1), and thrombin, were without effect on the proliferative activity of these neuronal cells. bFGF has no effect on the survival of motoneurons and on the fiber outgrowth of the whole neuronal population. However, bFGF affects the development of bipolar AChE-positive neurons, probably belonging to the non-motoneuron population. The data indicate that bFGF and aFGF are mitogens for neuroblasts from rat spinal cord in culture and that bFGF influences the development of a subpopulation of spinal neurons that are AChE-positive.
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PMID:Establishment of pure neuronal cultures from fetal rat spinal cord and proliferation of the neuronal precursor cells in the presence of fibroblast growth factor. 172 69

The effects of thrombin were examined in primary cultures of dissociated medial septal cells from fetal (embryonic day 17) rat brains. Seven days of continuous exposure of these cultures to thrombin produced a dose-dependent increase in the activity of the enzyme choline acetyltransferase (EC 2.3.1.6) and no change in the number of acetylcholinesterase (EC 3.1.1.7)-positive cells. Maximal induction of choline acetyltransferase activity occurred around 1-2 nM thrombin and was first detected after five days of treatment. In addition, thrombin promoted neuronal cell aggregation, proliferation of the astroglia, and changes in astroglial cell morphology. Neuronal aggregation was first noted after 24 h of treatment, while the proliferative response of the astroglia was first apparent after four days of treatment, slightly prior to the increase in choline acetyltransferase enzymatic activity. In order to see if the induction of the enzyme choline acetyltransferase was dependent upon the astroglial cell response, we included the anti-mitotic agent 5-fluoro-2'-deoxyuridine, to find that astrocyte proliferation, as well as thrombin-induced increase in choline acetyltransferase, were both abolished. In contrast, the aggregation of neurons was not affected. Finally, thrombin-induced changes in choline acetyltransferase could not be antagonized by immunoneutralizing anti-nerve growth factor antibodies and when thrombin was added simultaneously with 100 ng/ml 2.5-S nerve growth factor, the increase in choline acetyltransferase activity was additive. In conclusion, it appears that thrombin affects cholinergic septal neurons indirectly via the responsive astrocytes in a manner distinct from nerve growth factor.
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PMID:Thrombin indirectly affects cholinergic cell expression in primary septal cell cultures in a manner distinct from nerve growth factor. 175 63


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