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)

Electrolytic lesioning of the medial septum (MS) was used to assess the effectiveness of tacrine (THA) in reversing lesion-induced spatial memory deficits in a water-maze. Lesioned animals were injected with either 3 mg/kg or 5 mg/kg of THA intraperitoneally 15 min prior to daily behavioral training. One group of the lesioned and sham-operated animals received saline. All animals underwent two training trials each day for a period of ten days, after which a spatial probe trial was performed and assessed. The accurate placement of MS lesions resulted in lowered acetylcholinesterase (AChE) and choline acetyltransferase (ChAT) activity within the hippocampus of lesioned rats. Lesioning of the MS also impaired the learning performance in locating the escape platform during training and decreased the spatial bias during the probe trial. A lower dose of THA (3 mg/kg) significantly reversed the path length increase and spatial bias decrease induced by MS lesioning, but had no effect on escape latency. However, comparison between the saline- and THA- (5 mg/kg) injected MS-lesioned rats showed no significant differences in either escape latency or spatial bias. The present results support the use of cholinesterase inhibitors in further treatment trials of geriatric memory disorders.
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PMID:The effects of THA on medial septal lesion-induced memory defects. 235 95

Light and electron microscopic peroxidase-antiperoxidase immunocytochemistry has been used to localize choline acetyltransferase, substance P and enkephalin in the hypoglossal nucleus of the rat. Choline acetyltransferase immunoreactivity was observed in motoneurone cell bodies and proximal dendrites, in large varicosities in the surrounding neuropil and in nerve terminals in synaptic contact with immunostained motoneurones. Most choline acetyltransferase immunostained terminals which made synaptic contact with motoneurone cell bodies and proximal dendrites possessed prominent subsynaptic cisterns and belong to the terminal type referred to in the literature as C or L. Substance P and enkephalin immunoreactivity did not occur in motoneurones but was seen in fibres and synaptic terminals. Substance P immunoreactive fibres made multiple axosomatic contacts while enkephalin immunoreactive terminals made synaptic contact mainly with large and small dendrites. C terminals were not stained for either substance P or enkephalin. This study provides immunocytochemical support for the classic identification of hypoglossal motoneurones as cholinergic and in addition shows that these neurones are innervated by a number of morphologically and chemically distinct terminal types. C terminals have previously been shown to contain cholinesterase and our demonstration that these terminals contain choline acetyltransferase thus provides additional evidence for their cholinergic nature and for a cholinergic innervation of hypoglossal motoneurones. The origin of the immunoreactive terminals was not identified in this study but possible candidates include the raphe nuclei for substance P. and propriobulbar interneurones for choline acetyltransferase.
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PMID:Inputs to motoneurones in the hypoglossal nucleus of the rat: light and electron microscopic immunocytochemistry for choline acetyltransferase, substance P and enkephalins using monoclonal antibodies. 242 Nov 99

Incubation of cultured rat pituitary cell aggregates with [3H]choline ([3H]Chol) yielded a derivative that was identified as [3H]acetylcholine ([3H]ACh) by several criteria: 1) the [3H]Chol derivative with the highest retention time coeluted with a [14C]ACh standard in cation exchange and reverse phase HPLC; 2) cholinesterase treatment converted this derivative to a substance with the retention time of [3H]Chol; 3) two blockers of ACh production, hemicholinium and 4-[(1-naphthylvinyl)pyridinium], eliminated 3H-labeled material in the HPLC fractions with ACh retention time. Spontaneous [3H]ACh release was increased by depolarizing potassium concentrations, and both synthesis and release of ACh were increased by the glucocorticoid hormone dexamethasone. Double immunostaining of choline acetyltransferase (CAT) and, respectively, of ACTH, GH, PRL, TSH, S100, LH, and FSH in rat pituitary cells revealed that most of the CAT-immunoreactive cells were also ACTH immunoreactive. A small proportion (less than 10%) of the PRL-immunoreactive cells also showed CAT immunoreactivity, but all other cell types were negative. The immunocytochemical evidence for colocalization of CAT within the ACTH cell was strengthened by the finding of a significantly higher rate of [3H]ACh synthesis in a corticotroph-enriched cell population obtained by separating pituitary cells on a velocity sedimentation gradient. In addition, the mouse pituitary corticotropic cell line AtT20 contained CAT immunoreactivity, converted [3H]Chol to [3H]ACh, and released bioactive ACh-like material. In conclusion, the present data provide strong evidence that pituitary corticotrophs synthesize and release ACh, and that the activity of this intrapituitary cholinergic transmission system is under regulatory control.
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PMID:Synthesis and release of acetylcholine by normal and tumoral pituitary corticotrophs. 253 72

1. The onset and development of cholinergic mechanisms in the smooth muscle of the chick oesophagus were studied by estimating the changes in mechanical response and biochemical parameters between 9 days of incubation and 7 days after hatching. 2. Transmural and vagal nerve stimulation first evoked contraction in the oesophagus at 10 days and 11 days of incubation, respectively. These contractions were inhibited by atropine (1-2 microM) and potentiated by physostigmine (0.2 microM). On the other hand, hexamethonium (200 microM) had an inhibitory effect on vagal nerve stimulation but not on transmural nerve stimulation. 3. The relative amplitude of contraction induced by both vagal nerve and transmural stimulations compared to high K+ (80 mM)-induced contractions, progressively increased with age in embryos up to 19 days of incubation. 4. The activity of choline acetyltransferase (ChAT), an enzyme synthesizing acetylcholine (ACh), also gradually increased in the oesophagus during the period from 9 days to 19 days of incubation, which was similar to the change in the nerve-mediated contraction. On the other hand, the cholinesterase activity reached a maximum at 13 days of incubation and decreased until 7 days after hatching. 5. The contractile response to ACh and binding sites of [3H]-quinuclidinyl benzilate ([3H]-QNB) were observed in the oesophagus at 9 days of incubation. The maximum response produced by ACh (300 microM) tended to be greater in early stages (9-13 days of incubation) than in later stages. The sensitivity estimated from pD2 values increased up to 15 days of incubation. The maximum response produced by ACh (300 microM) tended to be greater in early stages (9-13 days of incubation) than in later stages. The sensitivity estimated from pD2 values increased up to 15 days of incubation. During the embryonic period, the number of muscarinic receptors estimated from the binding of [3H]-QNB changed very little. 6. These results suggest that in the chick oesophagus, extrinsic and intrinsic cholinergic innervation start to function at 10 days and 11 days of incubation, respectively and continue to develop progressively up to the time of hatching. It seems likely that the functional and biochemical maturation of receptive mechanisms on the smooth muscle precede those of cholinergic innervation.
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PMID:Development of cholinergic nerve transmission in the chick oesophagus. 254 45

Young adult rats received either unilateral or bilateral ibotenic acid infusions in their nucleus basalis, destroying most of the cholinesterase-staining neurons in that region. Cerebral cortex levels of choline acetyltransferase, somatostatin, neuropeptide Y, and monoamines were then assayed 2.5 and 10 months after bilateral lesions, or, 2.5, 10, and 14 months after unilateral lesions. Entorhinal and cerebral cortex levels of several amino acid transmitters were also measured. As expected, choline acetyltransferase activity was decreased in the frontal cortex ipsilateral to the ibotenic acid infusion in unilaterally or bilaterally lesioned animals. Parietal cortex concentrations of somatostatin and neuropeptide Y were altered by lesioning in a complicated, time-dependent manner. Thus, while unilateral lesions transiently decreased or had no effect on these neuropeptide levels, bilateral lesions elevated the level of each neuropeptide by over 100% at 10 months. Other cortical transmitter systems investigated appeared to be less affected by nucleus basalis-lesions. Unilateral lesions had no effect on prefrontal cortex norepinephrine, serotonin, or dopamine content at 14 months post-lesioning. These different neurochemical effects of unilateral and bilateral nucleus basalis lesions may be important for developing a model for the trans-synaptic effects of cortical cholinergic deafferentation.
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PMID:Different long-term effects of bilateral and unilateral nucleus basalis lesions on rat cerebral cortical neurotransmitter content. 257 19

Brief neonatal ethanol exposure (3.0 g/kg/dose, twice daily; postnatal day (PN) 4 to PN8) resulted in cholinergic neurochemical alterations in the cerebellum, but not the hippocampus of rats assayed on PN20. Analysis revealed that the binding affinity of cerebellar muscarinic receptors for [3H]quinuclidinyl benzilate was decreased by ethanol, but only in female pups. Other gender-specific but treatment-independent cerebellar differences were identified as well, including lower levels of choline acetyltransferase activity and S1-level (1,000 x g) crude protein in males and females, respectively. No evidence of ethanol-induced cholinergic change was noted in the hippocampus of the same pups on PN20. However, collapsed across treatment, male hippocampi were found to contain less S1-level protein than their female counterparts. Neither muscarinic receptor density nor acetyl cholinesterase activity were found to differ between treatments or genders, in either brain region. Consistent with the developmental timetables for regional cholinergic synaptogenesis in the rat, observations on PN20 confirm a hypothesis of cerebellar cholinergic vulnerability and hippocampal cholinergic resilience to neonatal ethanol insult.
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PMID:Exposure of rats to ethanol from postnatal days 4 to 8: alterations of cholinergic neurochemistry in the hippocampus and cerebellum at day 20. 268 69

The two parameters of the active [methyl-3H]choline uptake into isolated rat forebrain microvessels, Km and Vmax, were determined for 1-, 3-, 10-, and 24-month-old Charles River male rats and compared with the activities of the enzymes choline acetyltransferase (ChAT), acetylcholinesterase (AChE), and butyrylcholinesterase (BuChE) in these microvessels over the same time course. The value of Km remained constant over the entire period, but that of Vmax increased from 8.5 +/- 1.0 to 80.6 +/- 16.4 nmol g-1 (mean +/- SEM) over the first 3 months of life. Over the same period, the increase in ChAT activity, from an initial value of 7.1 +/- 1.6 to 10.2 +/- 0.3 nmol g-1 min-1, was not proportional to that of choline uptake. Levels of BuChE activity (0.9-1.3 mumol g-1 min-1) were almost unchanged throughout the entire 24-month period, but those of AChE showed a steady and significant increase from 1 to 24 months, remaining relatively high at senescence (4.7 mumol g-1 min-1), when choline uptake had decreased to one-third of its optimal value. Selective inhibition of AChE with 1,5-bis(4-allyldimethylammonium-phenyl)pentan-3-one dibromide (0.5 microM) in unruptured capillaries from 3-month-old rats resulted in a decrease in Vmax of choline uptake from approximately 81 to 59 nmol g-1 min-1 or with 9-amino-1,2,3,4-tetrahydroacridine (10 microM) in capillaries from 2-month-old rats from approximately 30 to 15 nmol g-1 min-1. Selective inhibition of BuChE with tetraisopropyl pyrophosphoramide (100 microM) resulted in an increase in Vmax from approximately 81 to 96 nmol g-1 min-1. It is possible that the two vascular enzyme systems are coupled to a hypothetical endothelial choline transporter, but with an action opposite to each other.
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PMID:Vascular cholinesterases and choline uptake in isolated rat forebrain microvessels: a possible link. 274 36

Mothers who smoke cigarettes during pregnancy give birth to babies with lower birth weights than do nonsmoking mothers. One hypothesis to explain this finding is that nicotine depresses the activity of the placental cholinergic system, which has been linked to the placental transport of amino acids and other substances. The levels and activities of several components of the term placental cholinergic system were determined in smokers and nonsmokers to investigate whether this system is involved in the effect of smoking. There were no statistically significant differences in the levels, synthesis or release of acetylcholine in the tissues from smoking and nonsmoking mothers, nor in the activities of the choline uptake system or the enzymes choline acetyltransferase, cholinesterase or sodium/potassium adenosine triphosphatase. The results do not support the hypothesis that the lower birth weights of babies born to smoking mothers is mediated by an effect of nicotine or other tobacco components on the placental cholinergic system.
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PMID:The effect of cigarette smoking during pregnancy on the cholinergic system in isolated term human placental tissue. 293 60

The distribution of acetylcholinesterase and choline acetyltransferase in primary visual areas of adult pigmented ferret was determined with cholinesterase histochemistry and choline acetyltransferase immunohistochemistry. In all visual areas the distribution of acetylcholinesterase in the neuropil closely matches that of choline acetyltransferase. In the cerebral cortex acetylcholinesterase and choline acetyltransferase are associated with axons found in every cortical layer and in the white matter. Area 17, identified by Nissl architectonics and cytochrome oxidase histochemistry, is distinguished by having a relatively low density of choline acetyltransferase- and acetylcholinesterase-stained axons in layer IV. Certain cortical non-pyramidal cell types show moderate staining for acetylcholinesterase after relatively long incubations, but no choline acetyltransferase-positive cells are observed in the cortex. In the lateral geniculate nucleus and superior colliculus the levels of choline acetyltransferase and acetylcholinesterase are considerably higher than in cerebral cortex, and choline acetyltransferase-stained axons there display prominent varicosities. The distribution of choline acetyltransferase and acetylcholinesterase in the neuropil of lateral geniculate nucleus and superior colliculus of ferret shows marked laminar variation. For instance, in the lateral geniculate nucleus, the levels of acetylcholinesterase and choline acetyltransferase in the "On" sublaminae of laminae A and A1 are higher than the "Off" sublaminae. In the superficial layers of the superior colliculus the levels of choline acetyltransferase and acetylcholinesterase are highest in the stratum zonale and lowest in the stratum opticum; in the intermediate gray layer of the superior colliculus acetylcholinesterase- and choline acetyltransferase-stained fibres are distributed into dense patches. As in cortex, choline acetyltransferase-positive cell bodies are not found in the lateral geniculate nucleus or superior colliculus, and acetylcholinesterase-stained cell bodies are visible only after long incubations. Cell bodies staining positively for choline acetyltransferase are found in a satellite of the superior colliculus, the parabigeminal nucleus.
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PMID:Cholinergic innervation of ferret visual system. 303 24

Monkeys with bilateral ibotenic-acid lesions of the nucleus basalis of Meynert, an area rich in cholinergic neurons that innervate the cerebral cortex, were compared with unoperated control monkeys on a recognition memory task. Although animals with large lesions had substantial reductions of cortical choline acetyltransferase activity, none showed impairment in the task. Lesion effects were observed, however, when performance was assessed following administration of a muscarinic receptor blocker (scopolamine) or a cholinesterase inhibitor (physostigmine). Although scopolamine produced dose-related impairments in both groups, this effect was greater in the experimental animals. Conversely, whereas physostigmine produced modest improvement in performance in the control group, no such improvement was observed in the experimental animals. The altered sensitivity to the mnemonic effects of cholinergic agents in the experimental group suggests that the cholinergic neurons of the nucleus basalis of Meynert contribute to recognition memory.
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PMID:Effects of scopolamine and physostigmine on recognition memory in monkeys with ibotenic-acid lesions of the nucleus basalis of Meynert. 311 81


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