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)

Cerebrospinal fluid acetylcholinesterase (AChE) activity was studied as a possible marker for central cholinergic neuronal function in seven patients with Gilles de la Tourette's syndrome. No significant differences were found between CSF AChE activity in untreated or haloperidol-treated patients and control populations. These data do not appear to support a pathophysiologic association between the cholinergic system and Gilles de la Tourette's syndrome.
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PMID:CSF cholinesterase activity in Gilles de la Tourette's syndrome. 658 29

The effect of various doses of pentylenetetrazol (PTZ) on the levels of dopamine-beta-hydroxylase (D beta H) and acetylcholinesterase (AChE) in the CSF of rabbits was studied. The drug augments in a dose-dependent manner the D beta H activity but causes only a small and dose-independent increase in AChE. This suggests that PTZ-induced convulsions are associated with an increase in central noradrenergic activity but not by an increase in central cholinergic activity.
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PMID:The effect of pentylenetetrazol on the levels of dopamine-beta-hydroxylase in the cerebrospinal fluid of rabbits: a dose-dependent relationship. 684 91

WEHI-3 cell-conditioned medium with the capacity to stimulate megakaryocyte colony formation was separated by Sephadex G-150 column chromatography. The development of colonies containing megakaryocytes was observed only when mixing experiments were performed. Individual fractions did not support megakaryocyte colony growth. The two factors in WEHI-3 CM required for megakaryocyte colony growth had apparent average molecular weights of 35,000 daltons (megakaryocyte CSF) and 100,000 daltons (megakaryocyte potentiator). The results were confirmed in serum-free conditions in which colonies were directly identified in the cultures by acetylcholinesterase staining. Two growth factors may be necessary for the genesis of megakaryocytic colonies.
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PMID:Two-factor requirement for murine megakaryocyte colony formation. 706 64

There is a growing body of evidence that the central nervous system (CNS), even in the adult animal, is capable of adaptation and reorganization not only as a result of partial damage to the CNS but also in response to stimulation. Environmental stimulation produces changes including expansion of visual cortex, increases in dendritic branching, glia and cholinesterase. Environmental stimulation also produces behavioural changes. Experimental electrical stimulation produces changes in synapse size, synaptic vesicle change, dendritic branching and changes in synaptic transmission. In man, repetitive electrical stimulation via epidural electrodes increases plasma levels of norepinephrine, epinephrine, and dopamine, and CSF levels of norepinephrine. Repetitive electrical stimulation in man dates back to 1967 and has been used for the control of pain, to improve spasticity, bladder control, motor deficit and the autonomic hyperreflexia of spinal cord injury. In addition, improvement has been reported in epilepsy, cerebral palsy, torticollis and peripheral vascular diseases. The best controlled studies are in multiple sclerosis and peripheral vascular disease, and these results will be presented in more detail.
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PMID:Rehabilitation following brain damage: some neurophysiological mechanisms. The effects of repetitive stimulation in recovery from damage to the central nervous system. 718 88

The aim of this study was to systematically characterize possible rhG-CSF effects on the murine megakaryocyte-platelet system (untreated and recovering from chemotherapy or extramedullary irradiation). In untreated, splenectomized male B6D2F1 mice, rhG-CSF treatment (50 micrograms/kg/d for up to 8 d) markedly decreased femoral megakaryocytopoiesis. CFU-Meg, small acetylcholinesterase-positive (SAChE) cells, and megakaryocytes were significantly reduced to 35-70%; platelets, however, were not affected. Peripheral CFU-Meg and CFU-GM increased up to 200-fold. Following a single injection of 5-FU (150 mg/kg) on day 0, rhG-CSF (50 micrograms/kg/d) on days 1-8 suppressed the megakaryocytopoietic recovery as indicated by significantly lower platelet numbers on day 9. Granulopoietic recovery was accelerated by rhG-CSF. When rhG-CSF treatment was started on day 5, no beneficial effect on granulopoietic recovery was observed, but again platelet levels were significantly lower on day 9, indicating that within the first 4 d of rhG-CSF application, recruitment or lineage competition was not a critical event. To test for the effects of extramedullary irradiation on circulating progenitors, mice pretreated with 50 micrograms/kg/d of rhG-CSF for 8 d received irradiation to the chest with 500 cGy resulting in a substantial kill of circulating CFU-Meg and CFU-GM of up to 99%. However, this striking decrease of blood progenitors did not significantly affect their total body contents. This study indicates that rhG-CSF treatment can impair bone marrow megakaryocytopoiesis, which might be an important consideration for those clinical situations that carry a high potential for treatment-induced thrombocytopenia.
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PMID:Effects of rhG-CSF, 5-fluorouracil and extramedullary irradiation on murine megakaryocytopoiesis in vivo. 752 38

Two experiments were conducted to assess the durability of nerve growth factor (NGF) effects on cholinergic neurochemical markers. Artificial CSF or NGF was infused via osmotic pumps for 2 weeks into the lateral ventricles of young adult (3- to 6-month-old) and aged (22- to 26-month-old) Fischer 344 rats. Assessment of choline acetyltransferase (CAT) and acetylcholinesterase (AChE) within the cortex, striatum, and hippocampus was conducted either approximately 3 (experiment 1) or 12 (experiment 2) weeks after termination of treatment. A variety of age-related deficiencies were found in the two experiments with decreased marker levels within the dorsal hippocampus and striatum being most consistent. NGF increased cholinergic marker enzyme activity in experiment 1 only. Specifically, NGF (a) attenuated age-related CAT and AChE deficits within the dorsal hippocampus and striatum, (b) enhanced CAT activity within the frontal cortex and ventral hippocampus in aged animals, and (c) increased CAT activity within the dorsal hippocampus in young subjects. It is concluded that NGF may be beneficial in enhancing cholinergic neurochemical parameters, especially in aged animals, but such effects are most likely transient.
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PMID:Transient enhancement of cholinergic neurochemical markers induced by NGF in aged F344 rats. 755 May 95

To date the evaluation of chemically-induced neurotoxic effects on humans has been dependent mostly on electrophysiological measurements, neurobehavioral tests and biological exposure assessment. However, recently attempts have been made to develop biochemical parameters in peripheral body fluids which can be easily obtained from humans and which can represent markers for the same parameters in nervous tissue. The approach of this kind is logically based on the following facts: 1) Blood cells (e.g., platelets and lymphocytes) possess some characteristics of monoaminergic neurons such as the existence of storage vesicles of monoamines, membrane neurotransmitter receptors, high affinity uptake sites and neurotransmitter-related metabolizing enzymes. 2) Leakage of nerve-specific markers from nervous tissue to peripheral body fluids may occur following damages of target neuronal cells or macromolecules. 3) Quantitative and/or qualitative alterations of peripheral biochemical markers (e.g. neurotransmitter receptors) can be induced by the regulation mechanisms of neuronal, endocrinal and immunologic interactions when the nervous functions are perturbed by various exogenous or endogenous factors. Erythrocyte acetyl cholinesterase (AChE), free erythrocyte protoporphyrin (FEP), lymphocyte neurotoxicity target enzyme (NTE), blood aminolevulinic acid dehydratase (ALA-D), and carboxyhemoglobin (CO-Hb) are well-known peripheral markers of the effects induced by organophosphates (AChE, NTE), lead (FEP, ALA-D) and carbon monoxide (CO-Hb). Many studies have been made on the effects of organic solvents, heavy metals and pesticides on neurotransmission parameters in blood cells such as neurotransmitter uptake, receptor binding and enzyme activity. This paper summarizes the present knowledge on the development and clinical applications of some peripheral biochemical markers such as neurotransmission parameters in blood cells and neuronal or glial cell marker proteins in CSF, blood and urine. The role of these peripheral biochemical markers in the assessment of environmental chemically-induced human neurotoxicity is also discussed.
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PMID:[The role of biochemical markers in peripheral body fluids in assessment of human neurotoxicity]. 791 53

The monoethylcholine aziridinium ion, AF64A, (3 nmol in 1 microliter) or artificial CSF (1 microliter) was infused unilaterally into the right dorsal lateral ventricle of male adult rats. Treatment with the L-type calcium channel antagonist, nimodipine (70 micrograms/kg b.wt.) or its vehicle was administered beginning before and for seven days following surgery. The infusion of AF64A reduced spontaneous alternation rates in the T-maze when compared to CSF and sham infused animals. AF64A-treated animals also took longer to reach the goal area in a complex maze task on specific trials relative to CSF and sham-infused animals. Locomotion and habituation to the open field did not differ between surgery groups. Unilateral AF64A significantly depleted acetylcholinesterase (AChE) positive terminals in the ipsilateral hippocampus and cell bodies in the ipsilateral medial septal area (MSA). Receptors for nerve growth factor (NGF-R), often colocalized with cholinergic cell bodies and terminals, also were depleted in the ipsilateral MSA of AF64A infused animals. Treatment with nimodipine did not have a neuroprotective effect on AF64A animals in either behavioral or histological results. However, some degree of protection was found in the vehicle-treated rats. This effect was likely a consequence of the stress of the injection procedure rather than the content of the vehicle, largely polyethylene glycol 400. Nimodipine-treated animals, regardless of surgery group, exhibited fewer emotional responses and had lower spontaneous alternation rates than untreated animals. The behavioral alterations found in the nimodipine groups are most easily explained in terms of altered emotionality. Overall our findings indicate that AF64A is a potent cholinotoxin that can selectively eliminate the ipsilateral septohippocampal cholinergic system when unilaterally infused into the lateral ventricle. It is possible that the mechanism of action of AF64A, like other nitrogen mustard analogues, involves disruption of basic processes involved in protein synthesis and DNA activities. Because of this, the toxic effects of the aziridinium mustard are independent of extracellular calcium and thus may not be susceptible to protection by calcium channel antagonists.
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PMID:Behavioral and neuroanatomical consequences of a unilateral intraventricular infusion of AF64A and limitations on the neuroprotective effects of nimodipine. 792 42

Cerebrospinal fluid acetylcholinesterase (CSF AChE) was determined for elderly delirious patients during the acute stage and after a 1- and 4-year follow-up periods, and the AChE levels were compared with age-equivalent controls. The AChE levels measured during the index admission correlated with the length of life after delirium, suggesting that cholinergic dysfunction may have prognostic significance in delirious patients. Although the CSF AChE concentrations measured during the index admission were in the same range as in controls, we observed a declining trend in patients with various structural brain diseases during the follow-up period. The decreasing levels may reflect the progression of the underlying dementia in these patients.
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PMID:A long-term follow-up study of cerebrospinal fluid acetylcholinesterase in delirium. 804 20

An improved high-performance liquid chromatographic (HPLC) method using electrochemical detection (ED) is described capable of routinely measuring the low levels of acetylcholine (ACh) typically found in rat brain microdialysis samples. Microdialysis was performed in the striatum of the urethane anesthetized rat using a 4-mm membrane length, high recovery (40% at 1.0 microliters/min; ambient conditions), loop-design probe perfused with an artificial cerebrospinal fluid (aCSF) solution containing physiologically normal calcium levels (1.2 mM). The HPLC method utilizes a polymeric stationary phase to resolve choline (Ch) from ACh. These analytes are then converted to hydrogen peroxide (H2O2) by a solid-phase reactor (containing immobilized choline oxidase and acetylcholinesterase enzymes). The H2O2 is detected amperometrically and quantitated on a platinum (Pt) working electrode (+300 mV; with a unique analytical cell featuring a solid-state palladium reference electrode). Two designs of the Pt working electrode were examined, differing only in the support material used (Kel-F or PEEK). The Kel-F/Pt electrode had a limit of detection (LOD) for both analytes of < 30 fmol per 10 microliters with a signal-to-noise ratio of 3:1. Striatal microdialysis perfusates were monitored for ACh and Ch over a 0-1000 nM range of neostigmine (NEO) in the CSF perfusion medium. Using the 4-mm probe, basal ACh and Ch levels were detected with a NEO level as low as 10 nM and were found to be 37 +/- 3 fmol and 22 +/- 1 pmol per 10 microliters (mean +/- S.E.M., n = 6 replicates) respectively. In similar experiments using 3-mm concentric probes comparable (lower) levels of ACh were found with the 50 and 1000 nM NEO doses (n = 4-21 animals). ACh could not be reliably quantitated when animals were perfused with the 10 nM dose of NEO (n = 4). The PEEK/Pt electrode had an improved LOD of < 20 fmol per 10 microliters due to a two- to three-fold decrease in the background noise component. Basal striatal levels of ACh in the absence of NEO approached the LOD and were found to be 15 +/- 2 fmol per 10 microliters; Ch was 5 +/- 1 pmol per 10 microliters (n = 2, mean of five basal samples). The analytical system requires very little maintenance; a simple electrochemical electrode cleaning step eliminates the need for routine polishing of the Pt electrode and the mobile phase is stable for up to one week.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Improved method for the routine analysis of acetylcholine release in vivo: quantitation in the presence and absence of esterase inhibitor. 815 Aug 61


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