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)

Partial ischemia of the spinal cord was produced by the ligature of the abdominal aorta twice for 40 minutes with a 40 min. recirculation interval. At the end of the ischemic period acetylcholinesterase (AChE. EC 3.1.1.7) activity increased significantly in the lumbosacral part of the spinal cord but simultaneously decreased in the spinal ganglia; There was no significant change in the sciatic nerve. After 48 hours of recovery AChE activity returned to normal in the sacral part of the spinal cord and in the spinal ganglia, but a less expressive increase remained in the lumbal part. Electrophoretic separation of AChE on the polyacrylamide gel gave in intact control dogs: three or four molecular forms in the spinal cord, five in the spinal ganglia and two molecular forms in the sciatic nerve. Ischemia increased the relative content of the lower molecular forms and often a new low molecular form appeared.
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PMID:Effect of ischemia on acetylcholinesterase activity and its molecular forms in the dog spinal cord, spinal ganglia and sciatic nerve. 721 Nov 50

We examined by morphological methodology the effect of (S)-N-ethyl-3-[(1-dimethyl-amino)ethyl]-N-methyl-phenylcarbamate hydrogentartrate (ENA-713), an acetylcholinesterase (AChE) inhibitor, on ischemia-induced neuronal death in the gerbil hippocampus due to a 5-min ligation of bilateral common carotid arteries after light ether anesthesia. Pyramidal cells had been decreased to 27% of sham-operated controls and the number of hypertrophic astrocytes expressing glial fibrillary acidic protein (GFAP) markedly increased in the hippocampal CA1 subfield 14 days after ischemia. However, post-ischemic administration of ENA-713 (three times 0.2 mg/kg, i.p.) significantly ameliorated this ischemia-induced decrease in the number of pyramidal cells by 47% of sham-operated controls, furthermore, it reduced the ischemia-induced accumulation of GFAP-positive astrocyte in the CA1 region. Together with previous results showing that ENA-713 protected against the ischemia-induced cholinergic abnormalities in the gerbil brain and improved cholinergic dysfunctions in the senescent rat brain, our present findings suggest that ENA-713 prove to be useful for treatment with senile dementia such as cerebrovascular dementia.
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PMID:Post-ischemic administration of the acetylcholinesterase inhibitor ENA-713 prevents delayed neuronal death in the gerbil hippocampus. 756 61

We designed the present study to examine whether or not the inhibition of acetylcholinesterase modulates cerebral microcirculation in hypotension and improves brain metabolism in ischemia induced by bilateral carotid artery occlusion in hypertensive rats. Blood flow to the parietal cortex was determined by the H2 clearance method. Lactate, pyruvate, and ATP were estimated by enzymatic methods. Acetylcholinesterase inhibitor (AChEI, ENA-713), at 0.05, 0.1, or 0.5 mg/kg, was intravenously injected 10 min before either hemorrhagic hypotension or cerebral ischemia. The levels of acetylcholine in the control were 29.3 +/- 8.1 (mean +/- SD) and 39.5 +/- 8.1 pmol/mg in the cortex and hippocampus, respectively, and they were significantly decreased by 15-19% after 60 min of ischemia in the vehicle-treated rats. AChEI preserved the levels to 93-98% of the control (p < 0.05 versus vehicle). The lower limit of autoregulation was 74 +/- 9% of the resting values. The administration of AChEI helped preserve blood flow and lowered the limit to 64 +/- 6% (p < 0.05 versus control). After 60 min of ischemia, lactate increased 6.5-fold and ATP decreased to 64% of the control value. The administration of AChEI dose-dependently reduced the lactate level 1.9- to 3.9-fold and well preserved the ATP level to 94-97% of the control. The inhibition of acetylcholinesterase activity may preserve cerebral autoregulation during hypotension and protect cerebral metabolism against ischemic insult.
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PMID:Inhibition of acetylcholinesterase modulates the autoregulation of cerebral blood flow and attenuates ischemic brain metabolism in hypertensive rats. 767 77

Motility disturbances following prolonged intestinal obstruction have been attributed to secondary effects. This study aimed to demonstrate the effects of incomplete obstruction on the enteric nervous system (ENS) of a rat model. Surgical placement of a nonstrangulating ligature encircling the distal bowel was performed in 41 freshly weaned rats. Anesthetic protocol included Ketamine, ether, or Xylazine (an alpha 2-adrenergic agonist). Histological evaluation was by ganglion cell morphology, histochemical staining for acetylcholinesterase (AChE) and tyrosine hydroxylase (TOH) immunocytochemistry. Forty-one freshly weaned LE rats were divided into controls (8), sham procedures (8), intestinal obstruction (16), and a group of rats with colonic biopsy performed prior to and following experimental obstruction (9). The rats were sacrificed at periods varying between 14 and 45 days post experimental obstruction (median survival, 27 days). Histological changes included elongation of ganglion cells and a decrease in the number per 5-mm slide in obstructed animals. No other obstruction specific differences were detected. A significant (P < .01) increase in AChE in the submucous plexus was recorded in Xylazine-anesthetized animals. No obstruction-specific effects could be demonstrated in the ENS, suggesting that prolonged obstruction without ischemia does not result in any significant alterations in the ENS. Pharmacological stimulation of the alpha 2-adrenergic receptor appeared to result in an increase in AChE. This mechanism may help to explain a possible role for the adrenergic system in the increased AChE levels in affected bowel in patients with Hirschsprung's disease.
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PMID:Secondary effects of prolonged intestinal obstruction on the enteric nervous system in the rat. 790 22

The effects of pre-treatment with ENA-713, an acetylcholinesterase (AChE) inhibitor, on changes in pre- and postsynaptic cholinergic indices in gerbil brain following transient ischemia were studied at 4 and 14 days after recirculation. In the ischemic group, hippocampal acetylcholine (ACh) level was significantly reduced (to 23% of sham-operated controls) at 4 days post-ischemia, but this reduction was completely prevented by ENA-713 treatment. Choline acetyltransferase (ChAT) and cholinesterase (ChE) activities were not significantly changed at 4 and 14 days post-ischemia. Although the maximum number (Bmax) of muscarinic ACh receptor (mACh-R) binding in the hippocampus was decreased (to 44%) without any change in affinity at 14 days post-ischemia, this decrease was also inhibited by ENA-713 treatment. In addition, histological experiment indicated that ENA-713 inhibited ischemia-induced pyramidal cell loss in the hippocampal CA1 regions. Thus, these findings suggest that ENA-713 has protective, neurotrophic and therapeutic effects on cerebrovascular type dementia due to cerebral ischemia.
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PMID:Acetylcholinesterase inhibitor ENA-713 protects against ischemia-induced decrease in pre- and postsynaptic cholinergic indices in the gerbil brain following transient ischemia. 818 20

The effects of a new acetylcholinesterase inhibitor, ENA-713, on ischemia-induced changes in acetylcholine, monoamines, and their metabolites, were studied in the gerbil. ENA-713 (0.2 mg/kg) or saline was administered intraperitoneally to gerbils 30 min before induction of cerebral ischemia by bilateral carotid occlusion. Pretreatment with ENA-713 mitigated the ischemia-induced abnormalities of the cholinergic, dopaminergic and serotoninergic systems in the gerbil brain, although it had virtually no effect on acetylcholine, monoamines, or their metabolites in any region of the normal gerbil brain. These findings suggest that ENA-713 has beneficial effects against ischemia-induced cerebral disorders. Thus, ENA-713 seems to be promising as a preventive or therapeutic agent for cerebrovascular dementia due to cerebral ischemia and might be useful for the treatment of Alzheimer-type dementia which is associated with multiple neurotransmitter abnormalities in the brain.
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PMID:Effects of the acetylcholinesterase inhibitor ENA-713 on ischemia-induced changes in acetylcholine and aromatic amine levels in the gerbil brain. 825 Jun 45

After small intestinal transplantation, intestinal isografts can organize migrating myoelectric complexes, and we have shown that migrating myoelectric complex frequency in the fasted state was reduced compared with controls after transplantation of the distal 50% of small intestine. We hypothesized that changes in motor activity after transplantation were related to alteration of cholinergic nerve activity or receptor density. With use of standard microsurgical techniques, the distal 50% of small intestine was orthotopically transplanted in a Lewis-to-Lewis donor-recipient combination. Resection controls were prepared by resecting the proximal 50% of small intestine, and sham controls were prepared by performing a sham laparotomy. Two months after surgery, small intestine was harvested. Choline acetyltransferase activity among the three groups was similar, suggesting that intrinsic cholinergic nerves remained intact. There was a strong trend toward decreased acetylcholinesterase activity [analysis of variance (ANOVA), P = 0.16] after transplantation, consistent with loss of extrinsic vagal nerve fibers. There were no differences in histochemical distribution of acetylcholinesterase among these groups. Muscarinic receptor density, as determined by binding to [N-methyl-3H]scopolamine, was decreased after transplantation (ANOVA, P = 0.02). There was a trend toward decreased receptor density in animals with resected small intestine. Surgical interruption of intrinsic nerve pathways rather than ischemia or extrinsic denervation might be the mechanism for diminished receptor density after transplantation, and reduced small bowel motor activity may be related to decreased density of muscarinic cholinergic receptors.
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PMID:Muscarinic cholinergic receptor density following small intestinal transplantation in rats. 827 56

Activities of choline acetyltransferase (ChAT) and acetylcholinesterase (AChE) were studied in the ventral and dorsal horns and the intermediate zone of the rabbit lumbar spinal cord (L4-7) 24 and 96 h after ischemia caused by 20 or 40 min occlusion of the abdominal aorta. Changes of AChE and butyrylcholinesterase (BChE) activities were also detected histochemically by the direct thiocholine method. No significant changes were found immediately after ischemia. The most remarkable change after 20 min ischemia and 1 or 4 d of reperfusion was heterogeneous decrease in ChAT and AChE activities in the examined parts of gray matter. The highest loss of enzyme activities was found in the ventral horns and the lowest in dorsal horns. Following 40 min ischemia and reperfusion the significant depletion in enzyme activities in all investigated zones of the gray matter was accompanied with necrotic degenerative changes. There was a relatively greater decrease in ChAT and AChE activities in the ventral horns that corresponded with a more prominent morphological damage of the cholinergic neurons in this zone of the spinal cord.
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PMID:Cholinergic enzymes in spinal cord infarction. Biochemical and histochemical changes. 839 88

Using a three-panel runway task, the effects of NIK-247 on impairment of working memory produced by scopolamine, hippocampal lesions, and cerebral ischemia were investigated in rats; these effects were compared with those of the well-known cholinesterase inhibitors, tetrahydroaminoacridine (THA) and physostigmine. Intraperitoneal injection of scopolamine (0.56 mg/kg) significantly increased the number of errors (pushes made on the two incorrect panels of the three-panel gates located at four choice points). NIK-247 (3.2-18 mg/kg PO), THA (1-10 mg/kg PO), and physostigmine (0.1 and 0.32 mg/kg IP) dose-dependently reduced the increase in errors induced by scopolamine. NIK-247 (32 mg/kg) was also effective in reducing the increase in errors produced by lesions of the dorsal hippocampus. A 5-min period of cerebral ischemia markedly increased the number of errors. NIK-247 (3.2 and 10 mg/kg), given immediately after blood flow recirculation and again 20 min before the runway test carried out 24 h after ischemia, significantly reduced the increase in errors expected to occur after ischemia. Tetrahydroaminoacridine (3.2 mg/kg) and physostigmine (0.1 mg/kg) similarly reversed the increased errors in ischemic rats. These results suggest that NIK-247 alleviates the impairment of working memory produced by scopolamine, hippocampal lesions, and cerebral ischemia, possibly through activation of the central cholinergic system.
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PMID:Ameliorative effects of the centrally active cholinesterase inhibitor, NIK-247, on impairment of working memory in rats. 843 69

The protective effect of regional epidural spinal cord cooling was evaluated in a rabbit spinal cord ischemia model. Hypothermia was performed by the continual perfusion of 2-4 degrees C cold saline in the epidural space around the ischemic lumbar segments, 4 min before and during ischemia. The spinal cord was deeply hypothermic (21 degrees C) throughout the whole ischemic period. Ischemia was induced by the occlusion of the abdominal aorta for 40 min under normothermic or hypothermic conditions. Recovery of motor and sensory functions, spinal cord-evoked potentials, and motor-evoked potentials were then evaluated up to 24 h postischemia. After this period, choline acetyltransferase (ChAT) and acetylcholinesterase (AChE) activities were measured, in particular, zones of the lumbar spinal cord. AChE was also investigated histochemically. Animals in the normothermic group displayed fully developed spastic paraplegia with near complete loss of spinal somatosensory and motor-evoked potentials. AChE histochemistry showed extensive necrotic changes affecting lumbosacral gray matter. These changes corresponding with the pronounced losses of ChAT and AChE activities indicated irreversible injury of the spinal cord. In contrast, after hypothermic ischemia, animals survived without any sign of neurological impairment with almost full recovery of the spinal cord-evoked potentials. ChAT and AChE activities in the gray matter showed near control values corresponding with histochemical analysis of fully preserved gray matter. Hypothermia under the present experimental conditions efficiently protected the spinal cord against ischemic injury.
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PMID:Epidural perfusion cooling protects against spinal cord ischemia in rabbits. An evaluation of cholinergic function. 853 29


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