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)

Angiotensin II and eledoisin modulate drinking behaviour in rats that is mediated by monoaminergic and cholinergic neurons. In the present study we have shown that combined intracerebroventricular injections of either 0.1 or 1.0 microgram doses of angiotensin and eledoisin resulted in a decrease of about 25-35% in activities of choline acetyltransferase, ATP-citrate lyase in the hippocampus. In addition, 1 microgram quantities of these peptides depressed activity of carnitine acetyltransferase but did not alter activity of acetylcholinesterase. On the other hand, the application of 0.1 microgram of angiotensin caused no change in activity of monoamine oxidase A, while 1.0 microgram dose brought about its 67% activation. Eledoisin abolished this effect of angiotensin II. These data provide evidence that angiotensin II and eledoisin evoke non related adaptive changes in cholinergic and monoaminergic neurons of the hippocampus.
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PMID:Effect of angiotensin II and eledoisin on cholinergic neurons in rat hippocampus. 161 Oct 32

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

The response of different types of skeletal muscle fibers to a snake venom PLA2 myotoxin was tested in vivo by injecting ACL myotoxin (ACLMT) into mice. Both the soleus (slow-twitch) and gastrocnemius (fast-twitch) were examined at different time periods (3 h, 3 and 21 d) after the injection. All animals received 5 mg/kg myotoxin into the subcutaneous lateral region of the right hind limb, near the Achilles tendon; contralateral muscles were used as controls. Cross-sections (10 microm) of frozen muscle tissue were cut from the medial region of the muscle. Alternate serial sections were stained either with toluidine blue or for acid phosphatase, myofibrillar ATPase activity after alkali (pH 10.3) or acid preincubation (pH 4.3), succinate dehydrogenase or acetylcholinesterase. Several stages of necrosis were observed 3 h after ACLMT injection, in both superficial and deep regions of both muscles. In these same regions 3 d after injection, clusters of regenerated muscle fibers were present, and some of them presented AChE activity. Twenty-one days after ACLMT injection the muscle fibers of soleus and gastrocnemius presented only chronic signs of damage such as split fibers and centralized nuclei. Using m-ATPase reactions it was possible to determine that both muscle fiber types I and II were injured in both muscles. The number of type IIC fibers was significantly increased, and the number of type II fibers significantly decreased in the gastrocnemius 21 d after ACLMT injection, suggesting a change in muscle fiber type from type II to type I, through type IIC. The increased number of type IIC fibers and the presence of AChE activity in clusters of regenerating fibers and split fibers indicate that injury by ACLMT produces axonal remodeling and muscle fiber type change.
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PMID:Injury and recovery of fast and slow skeletal muscle fibers affected by ACL myotoxin isolated from Agkistrodon contortrix laticinctus (Broad-Banded copperhead) venom. 969 Jul 94

Cholinergic hybrid mouse septal neurons SN56 were differentiated by separate and combined application of 0.001 mM all-trans-retinoic acid and 1 mM dibutyryl cAMP. Each of agents caused about twofold increase of choline acetyltransferase activity. These activatory effects were additive. Dibutyryl cAMP resulted in twofold increase of ATP-citrate lyase and acetylcholinesterase activities. Retinoic acid did not affect these enzyme activities but partially abolished activatory effects of dibutyryl cAMP. Pyruvate dehydrogenase and other enzymes of acetyl-CoA metabolism were not affected by this treatment. This work demonstrates that it is possible to rise cholinergic neurons of different expression of cholinergic and acetyl-CoA metabolism.
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PMID:Activities of enzymes of acetyl-CoA and acetylcholine metabolism in SN56 hybrid cholinergic cell line differentiated by dibutyryl cyclic AMP and all-trans retinoic acid. 983 4

The rate of acetylcholine (ACh) synthesis was found to depend on the activity of choline acetyltransferase (ChAT) and on the concentrations of the two substrates of this enzyme, choline and acetyl-CoA. In SN56 cells treated for 3 days with 1 mM dbcAMP activities of ChAT and acetylcholinesterase (AChE) were elevated. It was accompanied by an increased activity of ATP-citrate lyase (ACL)-an enzyme responsible for provision of part of acetyl-CoA for ACh synthesis in cholinergic neurons. In contrast lactate dehydrogenase (LDH) and pyruvate dehydrogenase (PDH) activities were reduced by dbcAMP. Treatment with 0.001 mM all-trans retinoic acid (RA) elevated ChAT and LDH activities but reduced the activities of AChE and ACL. The combined treatment with db-cAMP and tRA increased ChAT activity in supra-additive fashion. The effects of these two compounds on the other enzymes were not additive. Neither compound altered the activities of carnitine acetyl-transferase, acetyl-CoA synthase, or acetyl-CoA hydrolase. On the other hand, they decreased acetyl-CoA content and rate of ACh release. Overall, the results indicate that tRA upregulates only ChAT expression, whereas dbcAMP upregulates several features of cholinergic neurons including ChAT, AChE, and ACL. Low levels of acetyl-CoA in differentiated cells may result in a low rate of ACh release and resynthesis during their depolarization.
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PMID:Acetylcholine and acetyl-CoA metabolism in differentiating SN56 septal cell line. 1039 43

The aim of the present study was to reveal whether reduced cortical cholinergic input affects the acetyl-CoA metabolism in cholinoceptive cortical target regions which may play a causative role for the deficits in cerebral glucose metabolism observed in Alzheimer's disease. The effect of cortical cholinergic denervation produced by a single intracerebroventricular application of the cholinergic immunotoxin 192IgG-saporin, on activities of pyruvate dehydrogenase and adenosine triphosphate (ATP)-citrate lyase as well as on the level of synaptoplasmic and mitochondrial acetyl-CoA and acetylcholine release in cortical target regions was studied. Cholinergic lesion produced 83%, 72% and 32% decreases in the activities of choline acetyltransferase, acetylcholinesterase and ATP-citrate lyase in nerve terminals isolated from rat brain cortex, respectively, but no change in pyruvate dehydrogenase activity. Spontaneous and Ca2+-evoked acetylcholine release from synaptosomes was inhibited by 76% and 73%, respectively, following immunolesion. The lesion-induced 39% decrease of acetyl-CoA level in synaptosomal mitochondria was accompanied by 74% increase in synaptoplasmic fraction. Levels of acetyl-CoA and CoASH assayed in fraction of whole brain mitochondria from lesioned cortex were 61% and 48%, respectively, higher as compared to controls. The data suggest a preferential localization of ATP-citrate lyase in cholinergic nerve terminals, where it may contribute to the transport of acetyl-CoA from the mitochondrial to the cytoplasmic compartment. They provide evidence on differential distribution of acetyl-CoA in subcellular compartments of cholinergic and non-cholinergic nerve terminals. There are also indications that cholinergic activity affects acetyl-CoA level and its intracellular distribution in glial and other non-cholinergic cortical cells.
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PMID:Changes in cortical acetyl-CoA metabolism after selective basal forebrain cholinergic degeneration by 192IgG-saporin. 1451 Nov 9