Disease relevance of ACHE

• It was concluded that most of the AChE of the cat SCG is present in the plasma membranes of the preganglionic axons and their terminals, and in the dendritic and perikaryonal plasma membranes of the postsynaptic ganglion cells [1].
• Central respiratory depression induced by acetylcholinesterase inhibition: involvement of anaesthesia [2].
• Effect of cardiac arrhythmias & antiarrhythmic drugs on myocardial acetylcholinesterase in the cat [3].
• Reversal of the hypotension by HI-6 occurred irrespective of whether the organophosphorus agent was NBD-AP-MPF, which forms conjugates with acetylcholinesterase that undergo no aging, or soman, which forms conjugates that undergo extensive aging rendering the enzyme refractory to oxime reactivation [4].

Psychiatry related information on ACHE

• A second series of experiments demonstrated that mPRF microinjection of NLA significantly reduced the amount of REM sleep and the REM sleep-like state caused by mPRF injection of the acetylcholinesterase inhibitor neostigmine [5].
• Brain selective inhibition of acetylcholinesterase: a novel approach to therapy for Alzheimer's disease [6].
• Proactive and retroactive effects of hippocampal stimulation on active avoidance learning, hippocampal EEG and brain acetylcholinesterase activity in cats [7].

High impact information on ACHE

• If the cat caudate nucleus is stained for acetylcholinesterase a number of macroscopically visible zones appear that have lower acetylcholinesterase activity than the surrounding tissue [8].
• In vivo release of acetylcholinesterase in cat substantia nigra and caudate nucleus [9].
• Acetylcholinesterase like that of skeletal muscle in smooth muscle reinnervated by a motor nerve [10].
• Role of axoplasmic transport in neurotrophic regulation of muscle end plate acetylcholinesterase [11].
• Electron microscope localization of acetylcholinesterase and butyrylcholinesterase in the superior cervical ganglion of the cat. II. Preganglionically denervated ganglion [12].

Chemical compound and disease context of ACHE

• In confirmation of earlier light microscopic findings by the highly specific copper thiocholine method, there was nearly a total disappearance of AChE from the ganglion; no myelinated or unmyelinated axons with AChE-stained axolemmas were found, and only occasional traces of AChE staining were noted at dendritic and perikaryonal plasma membranes [12].
• We analyzed the activities of acetylcholinesterase and butyrylcholinesterase, and of the metabolic enzymes enolase and lactate dehydrogenase, in the superior cervical ganglion, ciliary ganglion, dorsal root ganglion, stellate ganglion, and caudate nucleus of the cat; we found that these tissues possess very different levels of enzymic activities [13].
• The effects of acetylcholine (ACh), the muscarinic antagonist scopolamine (Sco), the nicotinic antagonist dihydro-beta-erythroidine (DBE), and the acetylcholinesterase inhibitor physostigmine (Phy) on maintained and light-evoked ganglion cell discharge was examined using iontophoresis techniques [14].

Biological context of ACHE

• Addition of acetylcholinesterase (20 U/ml) to the superfusion medium did not change the membrane potential or the input resistance of the Purkinje cells [15].
• Based on dose-response experiments, we microdialyzed a 0.1 mM solution of the acetylcholinesterase inhibitor neostigmine into the L7 level of the dorsal horn of anesthetized cats to determine its effects on the mean arterial blood pressure (MAP) and heart rate (HR) responses to static muscle contraction or passive stretch [16].
• An inverse correlation exists between cell size and AChE activity [17].
• Comparisons were made among binding site distributions, acetylcholinesterase staining and tyrosine hydroxylase-like immunoreactivity in serial or neighboring nigral tissue sections [18].
• These findings show a down regulation of muscarinic receptors after DFP associated with low AChE activity [19].

Anatomical context of ACHE

• It is proposed that the maintenance of AChE at postsynaptic sites in normal ganglia is caused by the release of a trophic factor(s) from presynaptic terminals [12].
• As in the normal SCG, physostigmine-resistant staining, caused by noncholinesterase enzymes plus the possible presence of very low concentrations of AChE or BuChE, was noted at external mitochondrial membranes, elements of the endoplasmic reticulum of neurites and Schwann cells, and also in lysosomes [12].
• Serotonin 1C receptors and synaptic zinc were found to demarcate columns within layer IV of kitten visual cortex, which were interdigitated with a second, patchy system characterized by increased levels of cytochrome oxidase and acetylcholinesterase [20].
• These findings are consistent with the conclusion, drawn from a previous in vitro study, that glycyl-L-glutamine acts at a stage prior to the aggregation of the G1 form into higher polymers to maintain the acetylcholinesterase content of denervated ganglia [21].
• A detailed and striking match was found between these configurations and the compartmental distribution of acetylcholinesterase observed in the caudoputamen and ventral striatum of the same brains [22].

Associations of ACHE with chemical compounds

• We here report observations on the distribution of acetylcholinesterase (acetylcholine hydrolase, EC 3.1.1.7) in the striatum of the adult human, the rhesus monkey, and the cat [23].
• We observed an increased proportion of the globular monomeric G1 form, and to a lesser extent of the dimeric G2 and tetrameric membranous G4 forms, of acetylcholinesterase in the glycyl-L-glutamine-treated compared with the control cultures [24].
• Direct demonstration of a correspondence between the dopamine islands and acetylcholinesterase patches in the developing striatum [22].
• Because choline acetyltransferase, in contrast to acetylcholinesterase, occurs exclusively in the preganglionic axons and their terminals, this finding raises the possibility that glycyl-L-glutamine opposes postsectional axonal degeneration [25].
• There was only a small increase in the total acetylcholinesterase activity and no significant variation in the activity of the metabolic enzyme lactate dehydrogenase [24].

Other interactions of ACHE

• Glycyl-L-glutamine, a precursor, and glycyl-L-glutamic acid, a neurotrophic factor for maintenance of acetylcholinesterase and butyrylcholinesterase in the preganglionically denervated superior cervical ganglion of the cat in vivo [26].

Analytical, diagnostic and therapeutic context of ACHE

• The 24-hr intracarotid infusion of plasma-treated glycyl-L-glutamine (3 microM) produced significant enhancement of the monomeric G1 and tetrameric G4 forms of acetylcholinesterase of the cat superior cervical ganglion 48 hr after denervation, in comparison with denervated, noninfused controls [21].
• Ligation of the external carotid and lingual arteries at 24 hr postdenervation was found to oppose the preservation of acetylcholinesterase and butyrylcholinesterase contents of the ganglia induced by barbiturate anesthesia [27].
• When examined histochemically, cat and rabbit cerebral arteries exhibited a rich plexiform distribution of acetylcholinesterase which was not affected appreciably by sympathetic denervation [28].
• Occurrence of vasoactive intestinal polypeptide (VIP)-like immunoreactivity in certain cholinergic neurons of the cat: evidence from combined immunohistochemistry and acetylcholinesterase staining [29].
• Several light microscopic techniques including Golgi impregnations, Nissl stains, and acetylcholinesterase histochemistry were used, as well as electron microscopy [30].

References