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)

The levels of neurotransmitters and related metabolic enzyme activities in the brain of young-adult (3 months old), aged (11 months old) and nimodipine-administered (11 months old) senescence-accelerated mouse (SAM) were compared. Nimodipine, a calcium antagonist, was administered orally for 5 months. Acetylcholine (ACh), serotonin (5-HT) and dopamine (DA) levels all decreased with age but this decrease was attenuated by nimodipine. Choline acetyltransferase and choline esterase activities increased with age, and nimodipine enhanced their activities. Tryptophan hydroxylase activity was not affected by age or nimodipine administration. Monoamine oxidase-A activity increased with age, and was decreased by nimodipine administration. These results suggest that SAM rapidly undergoes neurochemical changes which are considered to be part of the normal aging process, and these changes were attenuated by chronic administration of nimodipine.
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PMID:Neurochemical changes related to ageing in the senescence-accelerated mouse brain and the effect of chronic administration of nimodipine. 756 56

We studied the effect of nimodipine (1000 ppm mixed in food), an L-type calcium-channel antagonist, administered for 4 months, on the cortical EEG activity in young and aged rats. Nimodipine treatment decreased cortical high voltage spindles (HVSs) in aged rats, but did not prevent the diminution of spontaneous locomotor activity. The threshold dose of metrifonate, a cholinesterase inhibitor, for suppression of HVSs was lower in nimodipine compared to placebo treated aged rats (30 mg/kg versus 60 mg/kg; p.o.). In young rats, nimodipine did not decrease HVSs, protect from scopolamine (0.1 or 0.8 mg/kg, i.p.) induced EEG slowing or augment the effect of metrifonate to suppress slow waves induced by scopolamine. The present results suggest that a chronic nimodipine treatment modulates thalamocortical arousal and thereby adds to the therapeutic effects of metrifonate to restore normal cortical electrical arousal in aged rats.
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PMID:Chronic nimodipine and acute metrifonate treatment decreases age-related cortical high voltage spindles in rats. 912 69

The present investigation was undertaken in order to study whether microvascular effects of the calcium antagonist nimodipine induces changes that can explain an increased detoxification of the highly toxic cholinesterase inhibitor soman. Anaesthetised, tracheotomised and artificially ventilated rats were treated intra-peritoneally (ip) with nimodipine, 10 mg kg(-1) or vehicle followed one hour later by the exposure to 45 microg kg(-1) soman (iv). Nimodipine per se induced a vasodilation in the intestine, myocardium and other muscles. In the abdominal skin soman elicited a significant vasoconstriction that was turned into an increased blood flow after nimodipine pre-treatment. A slight vasoconstriction in diaphragm of soman intoxicated rats was turned into a significant vasodilation by nimodipine pre-treatment. In the intestinal parts no effect of soman was detected. However, in nimodipine pretreated animals soman induced a significant vasoconstriction. The capacity of soman detoxifying processes, i.e. enzymatic hydrolysis and covalent binding to different esterases, is unequally distributed throughout the body. Together with the knowledge of the detoxifying processes of cholinesterase inhibition the results support our theory, that nimodipine alters the peripheral blood flow in a beneficial way resulting in improved detoxification ability.
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PMID:Nimodipine affects the microcirculation and modulates the vascular effects of acetylcholinesterase inhibition. 1464 25