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 (CSF) amino acid neurotransmitters, related compounds, and their precursors, choline levels, and acetylcholinesterase activity were measured in the CSF of patients with cerebellar ataxia during a randomized, double-blind, crossover, placebo-controlled clinical trial of physostigmine salicylate. The CSF gamma-aminobutyric acid, methionine, and choline levels, adjusted for age, were significantly lower in patients with cerebellar ataxia compared with controls. Physostigmine selectively reduced the level of CSF isoleucine and elevated the levels of phosphoethanolamine. No change occurred in CSF acetylcholinesterase activity and in the levels of plasma amino compounds in patients with cerebellar ataxia when compared with controls. Median ataxia scores did not statistically differ between placebo and physostigmine nor did functional improvement occur in any of the patients.
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PMID:Cerebrospinal fluid as a reflector of central cholinergic and amino acid neurotransmitter activity in cerebellar ataxia. 197 60

The effect of acetylcholinesterase inhibitors on free swim behavior in rats pretreated with scopolamine (0.32 mg/kg, IP) was examined. Long-Evans rats received a single 5-min testing trial in a 1.5 m black swimming pool, and swim distance in three concentric annulus corridors (peripheral, middle, and inner) and the number of body-turn transitions (greater than 45 degrees) were measured. Physostigmine (1.0 mg/kg, IP) increased swim distance in the middle and inner annulus corridors, compared to tetrahydroaminoacridine (2.0 mg/kg and 10 mg/kg, IP) and scopolamine alone (control) (Ps less than 0.01), and increased body-turn transitions, compared to all the other groups (Ps less than 0.05), but had no significant effect on peripheral annulus corridor swim distance, total swim distance, or swim speed. The results suggest that physostigmine produces uniquely different free swim patterns from tetrahydroaminoacridine following cholinergic blockade. These findings have implications for investigations attempting to restore spatial learning and navigation (e.g., Morris water maze) using acetylcholinesterase inhibitors following experimentally-induced cholinergic losses.
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PMID:Comparison of tetrahydroaminoacridine and physostigmine on scopolamine-induced free swim behavior in the rat. 202 24

The contractile responses of isolated and activated bovine retinal microarteries (BRA) (diameter, 204 +/- 4 microns; n = 48) to acetylcholine (ACh) were studied. These responses depended on the nature of the activating agent. The ACh relaxed BRA activated by prostaglandin F2 alpha (PGF2 alpha) and circumferential stretching in a dose-dependent manner but had no significant effect on K(+)-activated BRA. The effects of ACh also depended on the degree of BRA activation: the stronger the PGF2 alpha-induced contractions, the weaker the relaxation produced by ACh. In equivalent PGF2 alpha-induced contractions, the ACh effects were reproducible. The muscarinic antagonist, atropine, reversed the relaxation caused by ACh of PGF2 alpha-activated BRA. Physostigmine, an inhibitor of acetylcholinesterase, did not potentiate or prolong the relaxant action of ACh. Selective removal of the BRA endothelium (by gassing the BRA lumen, checked by scanning electron microscopy) blocked the relaxation caused by ACh of PGF2 alpha-induced contractions and unmasked a constricting action of ACh. This suggests that, in BRA with functional endothelium, the direct constricting effects of ACh on smooth muscle are masked by the more potent dilating activity, mediated by endothelial muscarinic receptors. Acetylcholinesterase was not found in BRA.
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PMID:Contractile responses of isolated bovine retinal microarteries to acetylcholine. 205 94

Physostigmine and tetrahydroaminoacridine (THA) have been reported to improve cognitive function in patients with Alzheimer's disease. Two experiments were conducted to examine the effects of these anticholinesterase agents on learning in aged rats pretreated chronically with barbital. In the first experiment animals received barbital in their drinking water for 46 weeks. Controls were given only water. On days 100-104 of abstinence, when the animals were 20 months old, acquisition of the Morris maze task was initiated after treatment with physostigmine. It was found that physostigmine improved learning of the maze task in control but not barbital treated rats. In the second experiment animals received barbital solution or water as in experiment one. On days 100-103 of abstinence they were injected with THA before being tested in the Morris water maze. It was found that THA improved learning in both barbital treated and control rats. These results corroborate clinical findings of improved cognitive function following treatment with THA, and suggest that the therapeutic effects of THA may be mediated by mechanisms distinct from cholinesterase inhibition. Furthermore chronic barbital treatment could be used as a model to study cognitive disturbances in experimental animals.
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PMID:Learning deficits in aged rats pretreated chronically with barbital and tested late in abstinence: alleviation by tetrahydroaminoacridine. 207 8

Physostigmine is considered to be a potential pretreatment agent against organophosphate intoxication. This investigation elicits the effects of three intensities of acute exercise (50, 80 and 100% VO2max), administration of physostigmine (70 micrograms/kg, i.m.) and the combined effect of physostigmine and three intensities of acute exercise on cholinesterase activity in red blood cells and various tissues and endurance time in rats. The cholinesterase activity in red blood cells in exercised rats not exposed to physostigmine was significantly greater than that of unexercised controls (116, 112 and 108% of control, p less than 0.05, at 50, 80 and 100% VO2max, respectively) while in other tissues the cholinesterase activity in general decreased slightly. In unexercised rats given physostigmine, the cholinesterase activity ranges were 73-79, 66-68, 68-74, 67-81 and 57-61% of controls from 10-30 min in red blood cells, brain, heart, diaphragm and thigh muscle, respectively. In exercised rats exposed to physostigmine, the cholinesterase activity ranges were 54-51, 58-50, 77-73, 71-83 and 54-58% of controls from 10-30 min in red blood cells, brain, heart, diaphragm and thigh muscle, respectively. The results indicate that in control rats not given physostigmine, different intensities of acute exercise affect the cholinesterase enzyme to a moderate degree in red blood cells (p less than 0.05) and heart (p less than 0.05) without affecting brain, diaphragm and thigh muscle. Acute exercise modifies the effect of physostigmine significantly (p less than 0.01) by increasing the cholinesterase inhibition in red blood cells and brain without affecting other tissues. Exposure of rats to physostigmine (70 micrograms/kg, i.m.) increases the endurance time in rats (160-200 g weight), possibly due to peripheral vasodilatation and lowering of core temperature.
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PMID:Interactive effects of physostigmine and exercise on cholinesterase activity in red blood cells and tissues of rat. 209 16

The optical isomer (+)Physostigmine [(+)Phy] is a very weak anticholinesterase. In a recent report, pretreatment with (+)Phy, at a dose which failed to inhibit acetylcholinesterase (AChE), and atropine provided efficacy against a lethal dose of sarin (SYNAPSE:2, 139, 1988). It was of interest to see whether (+)Phy could protect against soman at a dose which caused only marginal inhibition of the whole blood (WB) AChE in guinea pigs (GPs). (-)Phy (0.15 mg/kg, im) and (+)Phy (10.0 mg/kg, im) produced nearly 70% inhibition of WB AChE at 30 min whereas (+)Phy (0.15 mg/kg, im) caused only marginal inhibition. Groups of guinea pigs (20/group) were dosed, im, with (-)Phy (0.15 mg/kg), (+)Phy (0.15 mg/kg), (+)Phy (10.0 mg/kg) or vehicle (0.5 ml/kg) respectively in one thigh while the mild anticholinergic trihexyphenidyl (THP), 2.0 mg/kg, was injected into the other thigh of 10 animals from each of the respective groups. Thirty min after pretreatment, all animals were challenged with soman (60 micrograms/kg, sc; 2 LD50s); this dose of soman is lethal in unprotected animals. (-)Phy or (+)Phy (10 mg/kg) alone protected nearly 50% from soman lethality, and in combination with THP, all animals survived. In contrast, (+)Phy (0.15 mg/kg; alone or together with THP) was completely ineffective against a 2 LD50 challenge of soman. These data support the hypothesis that protection against soman-induced lethality is related to the degree of carbamylation of the AChE just prior to challenge.
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PMID:Acetylcholinesterase inhibition by (+)physostigmine and efficacy against lethality induced by soman. 227 42

Physostigmine, as a pretreatment candidate for nerve agent poisoning, was examined for cardiopulmonary side effects. Cardiovascular and pulmonary parameters were monitored in unanesthetized domestic pigs which received pulmonary arterial infusion of 5 micrograms/kg/min physostigmine salicylate for 2 hr. A level of 74% inhibition of red blood cell (RBC) acetylcholinesterase (AChE) activity was attained in 45 min, and this level of carbamylation increased only slightly during the remaining infusion period. In addition to this large change in AChE activity, minor changes were observed in hematocrit, heart rate, body temperature, mean aortic pressure, pulmonary arterial wedge pressure, and pulmonary artery pressure. Typically, these parameters showed a trend toward elevated levels. Blood gases, pH, respiratory rate, tidal and minute volume, cardiac output, nonelastic resistance, and dynamic compliance were not significantly different from baseline values. The unanesthetized pig responds to physostigmine in a manner similar to that reported for other species and appears to be a suitable model for evaluating cardiopulmonary effects of cholinesterase inhibitors.
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PMID:Effects of physostigmine on the cardiopulmonary system of conscious pigs. 230 26

Behavioral effects of nicotine and cytisine, and the cholinesterase inhibitors physostigmine and 9-amino-1,2,3,4-tetrahydroacridine (THA), administered intrathecally (IT) at the lumbar level in the rat have been evaluated. Antinociceptive dose relationships were established using the tail immersion test. Total activity, locomotion and rearing were also measured in computerized test boxes. The nicotinic receptor antagonist, mecamylamine, and the muscarinic receptor antagonist, atropine, were used to study the selectivity of the effects. Physostigmine and THA significantly decreased total activity, locomotion and rearing as compared to control animals. The motor effects of physostigmine were completely antagonized only partly. Mecamylamine had no antagonistic effect. Nicotine did not affect any activity parameter. Cytisin reduced total activity and locomotion 1-6 min after dose. IT physostigmine, 15 micrograms, increased tail immersion latency for 30 min. No significant increase in response latency in this test was observed after the IT administration of nicotine or THA, whereas cytisine elicited a small increase. The IT administration of THA, nicotine and cytisine was also associated with gnawing, vocalization and hyperactivity and in the case of THA, diarrhoea. These effects were blocked by mecamylamine. Physostigmine antinociception as well as the behavioral effects including total activity, locomotion and rearing caused by physostigmine and by THA are most probably due to an action on spinal muscarinic receptors. Nicotinic receptors do not seem to be involved in spinal antinociception. Some aversive behavioral effects caused by the IT administration of nicotinic receptor agonists could, however, be attenuated by the spinal administration of the antagonist mecamylamine, which may indicate the involvement of nicotinic receptors in afferent sensory transmission.
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PMID:Behavioral effects after intrathecal administration of cholinergic receptor agonists in the rat. 232 Jul 7

The purpose of this study was to see if physostigmine, a reversible cholinesterase inhibitor, affects the secretion and composition of saliva of the major salivary glands of the rat. Low doses of physostigmine did not elicit secretion. At higher doses there was significant flow from the parotid and submandibular glands within 5 min; however, no sublingual secretion was observed. The submandibular flow rate was highest for the first 5 min, then declined rapidly. The parotid flow rate initially was one-fifth of the maximum submandibular rate and then gradually decreased. The concentrations of Ca, Na and K of physostigmine-induced parotid saliva, and the Na of submandibular saliva, were similar to those with carbachol stimulation. The Ca and K concentrations of submandibular saliva were significantly higher than with carbachol or parasympathetic stimulation, and resembled those of alpha-adrenergic stimulation. The protein concentrations of physostigmine-evoked saliva from both glands were similar. The amylase activity of physostigmine-evoked parotid saliva was much higher than that of carbachol or parasympathetic stimulation. Physostigmine-evoked secretion was completely blocked by atropine, a cholinergic antagonist, and by reserpine, partially blocked by phentolamine, an alpha-adrenergic antagonist and not affected by surgical sympathectomy. Morphologically, physostigmine resulted in a moderate decrease in the number of acinar, but not ductal, secretory granules of both the parotid and submandibular glands, while the sublingual gland was unaffected. Numerous patches of parotid acini also developed vacuoles or vesicles. These results suggest that physostigmine-induced salivary secretion is mediated primarily by direct effects on cholinergic and alpha-adrenergic receptors.
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PMID:Physostigmine-induced salivary secretion in the rat. 235 Feb 65

Physostigmine (PH), alone, and pyridostigmine (PY), in combination with atropine and 2-PAM, have been shown to protect animals against organophosphate poisoning. While acute administration of either of these carbamates increased heating rates and decreased endurance of exercising rats, chronically administered PY did not induce these decrements, and we hypothesized that chronic administration of PH could also result in similar attenuation of these effects. Thus, PH was administered acutely (iv) or chronically (osmotic mini-pump) in the following 4 groups (510-530g, male, N = 10/group): C (control, saline iv), AC-200 (acute, 200 ug/kg, 58% whole blood cholinesterase (ChE) inhibition), CH-7 (chronic, 125 ug/hr, 7 days, 60% inhib.), and CH-14 (chronic, 125 ug/hr, 14 days, 56% inhib.). Rats were run (11 m/min, 26 degrees C) to exhaustion. The run times and heating rates (% of control) were: AC-200 - 47, 213%; CH-7 - 60, 157%; CH-14 - 92, 109%. Additionally, ultrastructural changes noted in diaphragms of acutely treated animals were less evident in chronically treated animals. Thus, the decremental effects of acute PH administration on endurance, thermoregulation, and ultrastructure were attenuated with chronic administration at similar levels of ChE inhibition.
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PMID:Chronic vs acute carbamate administration in exercising rats. 238 34


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