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)

Choline acetyltransferase (ChAT) and acetylcholinesterase (AChE) activity measured in the ventral and dorsal part of the dog spinal cord (L6-S2) and in the stumps of the sciatic nerve 5, 10, 15 and 21 days after its transection were compared with the corresponding activities in the intact contralateral nerve and in sham-operated animals. AChE was also examined histochemically. Changes in the enzyme activities in the central nerve stump were correlated with activity changes in the spinal cord. In the central nerve stump, a marked (25%) increase in AChE activity was found on the fifth day after transection, but by the 21st day it fell below control value levels; up to the 15th day it showed good correlation with AChE activity in the ventral spinal cord. Histochemically, pronounced reduction of enzymatic activity was found in the ipsilateral part of the spinal cord. On the 15th day, ChAT activity in the ventral spinal cord was also significantly decreased and the accumulation of the enzyme in the central nerve stump was negligible. On the contrary, at the last 21-day interval examined, a significant increase in ChAT activity and a nonsignificant increase in AChE activity was found in the spinal cord, but their activities in the central nerve stump were decreased. In the degenerated peripheral nerve stump ChAT activity dropped by an average of 99% and AChE activity by 48% during the first 15 days after transection but, on the 21st day, AChE activity was 22% higher than at the preceding interval.
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PMID:Effect of axotomy on cholinergic enzyme activities in the spinal cord and sciatic nerve of the dog. 295 37

The activities of acid phosphatase, hexosaminidase, beta-galactosidase, Mg2+-stimulated Na+K+ATPase, fumarase and ATP:citrate lyase were measured in grey matter of rabbit spinal cord 7-8 days after intra-ventricular or intra-cisternal injection of aluminium. RNA, DNA, and water content were measured in whole spinal cords. Choline acetyltransferase (CAT) and acetylcholinesterase were assayed in dorsal grey matter of the cord, which contained no aluminium-induced neurofilament accumulations (NFAs), and ventral grey matter, which had large numbers of such NFAs. CAT was also assayed in the hypoglossal nerve. None of these measures were consistently altered in the aluminium treated rabbits, although the activity of beta-galactosidase was increased in the NFA-free caudate nucleus of rabbits given aluminium intra-ventricularly, possibly due to the presence of phagocytes on the ventricular surface of the caudate. It is concluded that neither aluminium nor its induced NFAs has a gross effect on neuronal metabolism within 7-8 days.
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PMID:Biochemical studies on rabbits with aluminium induced neurofilament accumulations. 298 21

Effect on salivary secretion of a single dose and of chronic treatment with trithio-p-methoxyphenylpropene (anethole trithione; ANTT) was investigated in mice, rats and rabbits in relation to changes in function of the autonomic nervous system. Chronic treatment with ANTT enhanced salivary secretion induced by pilocarpine or electrical stimulation of the parasympathetic nerve, but had no effect on salivary secretion induced by isoproterenol or phenylephrine. A single dose of ANTT had no effect on salivary secretion. Chronic treatment with ANTT prevented the inhibition of parotid salivary secretion caused by atropine in rabbits. Choline acetyltransferase and acetylcholinesterase activities in rat submaxillary glands were not affected by chronic treatment with ANTT. These results suggest that chronic treatment with ANTT may enhance salivary secretion by stimulating the postjunctional secretory process involved in the parasympathetic nervous system.
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PMID:Enhancement of salivary secretion by chronic anethole trithione treatment. 323 51

Although the optic tectum of nonmammalian vertebrates has been extensively studied anatomically, there is little information about the identification of neurotransmitters and the enzymes critical to their synthesis. Choline acetyltransferase (ChAT), the enzyme responsible for acetylcholine synthesis, is presently regarded as the most reliable marker for cholinergic neurons, and its localization within putative cholinergic neurons has been made possible by the development of antibodies specific to ChAT. We have compared the immunocytochemical localization of ChAT to the histochemical staining of acetylcholinesterase (AChE) in the goldfish optic tectum. Goldfish brains reacted with the monoclonal antibody AB8 to ChAT have revealed that: (1) type XIV neurons are the only ChAT-positive cells in the tectum, and there are approximately 15,000 such cells per tectal hemisphere; (2) these neurons and other ChAT-containing afferent fibers form bands of label which correspond to those seen after AChE staining, and (3) many AChE-stained neurons do not contain ChAT. The immunohistochemical localization of ChAT has provided a direct method for determining the localization and organization of putative cholinergic structures in the optic tectum of goldfish. Future studies may elucidate the relationship of these cholinergic systems to the retinotectal projections, as there is close correspondence between AChE and ChAT location and the retinotectal termination patterns.
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PMID:Comparison of acetylcholinesterase and choline acetyltransferase staining patterns in the optic tectum of the goldfish Carassius auratus. A histochemical and immunocytochemical analysis. 331 Dec 87

Choline acetyltransferase (ChAT) and acetylcholinesterase (AChE) activities were determined in several brain regions of normal and streptozotocin-induced diabetic rats. The diabetic rats exhibited significant increase in ChAT activity (p less than 0.05) in all brain regions studied except for the cortex and the midbrain. Meanwhile, the diabetes condition was associated with significant increase (p less than 0.05) in AChE activity of the bulbus olfactorius, medulla oblongata and cerebellum. These data suggest that uncontrolled diabetes is associated with significant alterations in the brain cholinergic systems.
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PMID:Effect of diabetes on the enzymes of the cholinergic system of the rat brain. 341 89

Male Sprague-Dawley rats maintained under controlled environmental conditions were used. Choline acetyltransferase (ChAT) and acetylcholinesterase (AChE) activities were determined in the cerebral cortex, bulbus olfactorius, midbrain, hypothalamus, hippocampus, cerebellum, pons and medulla oblongata of control rats and rats treated with apomorphine (15 mg/kg, i.p.) after a single dose or after a second dose administered 24 h later at 10.00 or 22.00 h. Results of this experiment indicate that the repeated administration of apomorphine at 10.00 h was associated with rapid development of tolerance to the hypothermic action of this drug. A single injection of apomorphine resulted in significant (p less than 0.01) decrease of AChE and significant increase of ChAT activity (p less than 0.01) in the cortex, hypothalamus and pons. There were no significant differences between tolerant and control animals in the activities of AChE or ChAT in the bulbus olfactorius, cerebral cortex, midbrain, pons or medulla. On the other hand, repeated administration of apomorphine at 22.00 h was not associated with tolerance to the hypothermic action of this drug. A single injection of apomorphine at 22.00 h resulted in significant (p less than 0.01) increase in AChE activity of the midbrain, hippocampus, and the medulla oblongata with no significant changes in the cerebral cortex and bulbus olfactorius. There was a significant decline (p less than 0.01) of ChAT activity of the hypothalamus, hippocampus, cerebral cortex and the medulla oblongata (p less than 0.05). Meanwhile, there was a significant (p less than 0.05) increase of ChAT activity of the midbrain with no significant changes in the cerebellum, pons and the bulbus olfactorius.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Brain cholinergic involvement in the diurnal variations of the rapid development of tolerance to the hypothermic effect of apomorphine. 342 Jan 64

Inbred Wistar-Kyoto rats which are behaviorally more reactive to stress have a shorter life span than Brown-Norway rats. This is paralleled by higher basal activity and more pronounced changes in the septohippocampal cholinergic system of Wistar-Kyotos after stress. Age- and strain-dependent differences were therefore characterized in the septohippocampal system of 3- and 24-month-old (aged) Wistar-Kyotos and Brown-Norways, and in 30-month-old Brown-Norways. High affinity [3H]choline uptake and newly synthesized [3H]acetylcholine release served as markers for cholinergic terminals in the hippocampus. [3H]Quinuclidinylbenzilate binding served as a marker of muscarinic receptors in the hippocampus. Choline acetyltransferase activity served as a marker for cholinergic neurons and their terminals in the septum and hippocampus respectively. Acetylcholinesterase histochemical staining served to localize cholinergic neurons and their terminals in the septum and hippocampus respectively. In the hippocampus of aged Wistar-Kyotos choline uptake and acetylcholine release were reduced by approximately 50% compared to their young counterparts, but remained unchanged in aged Brown-Norways. Hippocampal choline acetyltransferase activity, acetylcholinesterase staining and muscarinic binding were unchanged in aged rats of both strains. Pyramidal cell loss (observed in Cresyl violet stained sections) was detected in hippocampus of 24-month-old Wistar-Kyotos and 30-month-old, but not younger Brown-Norways. Numbers of acetylcholinesterase-stained cells in the septum were reduced by 45 and 25% in 24-month-old Wistar-Kyotos and Brown-Norways respectively, and by 50% in 30-month-old Brown-Norways. Mean diameter of these cells was increased only in aged Wistar-Kyotos (approximately 46%) and in 30-month-old Brown-Norways (40%). The results indicate: (1) there is an ongoing age-dependent degeneration of septohippocampal cholinergic neurons which is associated with two principal compensatory changes in remaining cholinergic neurons: (a) hypertrophy of perikarya and (b) relative increase in activity of presynaptic markers in terminals with unchanged regional distribution, suggesting possible collateral sprouting; (2) age-dependent loss of septal cholinergic neurons precedes loss of hippocampal pyramidal neurons and (3) loss of pyramidal neurons in the hippocampus is associated with a compensatory increased muscarinic binding by remaining target hippocampal neurons. The results imply that higher basal and stress-induced activity of septohippocampal cholinergic neurons may be correlated with an accelerated and more pronounced age-dependent degeneration of this cholinergic system.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Age-dependent loss and compensatory changes of septohippocampal cholinergic neurons in two rat strains differing in longevity and response to stress. 343 31

In this study, male Sprague-Dawley rats maintained under controlled environmental conditions were used. Choline acetyltransferase (ChAT) and acetylcholinesterase (AChE) activities were determined in cerebral cortex, bulbus olfactorius, midbrain, hypothalamus, hippocampus, cerebellum, pons and medulla oblongata in control rats and rats treated with morphine (10 mg/kg) for 1 or 2 days. Repeated administration of morphine was associated with a decline in the degree of analgesia produced. Significant increase (p less than 0.01) in AChE activity of the medulla oblongata was observed following morphine administration for 1 or 2 days. A single injection of morphine resulted in a significant decline (p less than 0.01) in ChAT activity of hypothalamus, cerebellum and medulla oblongata. However, no such decline could be observed after 2 consecutive daily injections of morphine. In the cerebral cortex there was a significant decline (p less than 0.01) in ChAT activity after the second administration of morphine. These findings indicate that the changes in the responsiveness of the brain cholinergic enzymes following repeated morphine administration may in part explain the rapid development of tolerance to the analgesic effect of morphine.
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PMID:Brain cholinergic involvement during the rapid development of tolerance to morphine. 358 57

Choline acetyltransferase (ChAT) immunocytochemistry, acetylcholinesterase histochemistry and muscarinic receptor autoradiography demonstrated a cholinergic innervation within the superior colliculus. A method for the concurrent visualization of ChAT and transported horseradish peroxidase showed that a major extrinsic source for this cholinergic input is in the parabigeminal nucleus. We have designated these cholinergic neurons as the Ch8 cell group.
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PMID:Cholinergic projections from the parabigeminal nucleus (Ch8) to the superior colliculus in the mouse: a combined analysis of horseradish peroxidase transport and choline acetyltransferase immunohistochemistry. 370 16

Damage to the neocortex, here induced by the excitotoxin kainic acid in the rat, is known to induce cell shrinkage, without actual loss of cells, in the part of the cholinergic basal nucleus projecting to the damaged area. Fetal cortical tissue, implanted into the neuron-depleted cortex in the form of a dissociated cell suspension, completely prevented this degenerative change of the basal nucleus cholinergic neurons. Choline acetyltransferase biochemistry and acetylcholinesterase fiber staining of the transplants indicated a substantial ingrowth from the cholinergic host neurones into the graft. It is proposed that the basal forebrain cholinergic neurons normally receive a trophic influence from their target areas and that grafted neocortex can substitute for the loss of such trophic influence in cortex-damaged animals.
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PMID:Cortical grafts prevent atrophy of cholinergic basal nucleus neurons induced by excitotoxic cortical damage. 373 Aug 84


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