Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.1.1.8 (cholinesterase)
 12,691 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The innervation of the nasal septum and around the olfactory bulb has been investigated in rats by means of whole-mount preparations and histological sections. Silver staining, OsO4 staining, PAS staining, cholinesterase reaction and fluorescence for catecholamine-containing nerves were used. The nervus terminalis forms on the medial side of the olfactory bulb a ganglionated plexus, from which branches are given off which course peripherally with the vomeronasal nerves. From a dorsal part of the terminalis nerve plexus an anterior branch is given off which runs along the anterior ethmoidal nerve to the nasal vestibule where it connects with a group of ganglia. The peripheral branches of the nerve run from here along two epithelial cristae formed histologically like dermal papillae. Ventrally in the respiratory region at the junction of the nasal cavity and the nasopharynx is a 1 times 2 mm area with olfactory epithelium, glands of Bowman and an independent innervation from the olfactory bulb. This is the so-called septal olfactory organ. Trigeminal nerves form a plexus in the respiratory region and in the vestibule, but do not supply the olfactory region. Catecholamine-containing and cholinesterase-positive nerves run along the meningeal arteries on the cribriform plate and accompany their branches to the vascular plexus in the olfactory and respiratory regions. Double innervation is found not only of this vascular plexus but of the venous sinuses in the swell bodies of the vestibule. The glands of the nose are not surrounded by catecholamine-containing nerves.
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PMID:Demonstration of terminalis, olfactory, trigeminal and perivascular nerves in the rat nasal septum. 111 13

The distribution of 125I-neurotensin binding sites was compared with that of acetylcholinesterase reactivity in the human basal forebrain by using combined light microscopic radioautography/histochemistry. High 125I-neurotensin binding densities were observed in the bed nucleus of the stria terminalis, islands of Calleja, claustrum, olfactory tubercle, and central nucleus of the amygdala; lower levels were seen in the caudate, putamen, medial septum, diagonal band nucleus, and nucleus basalis of Meynert. Adjacent sections processed for cholinesterase histochemistry demonstrated a regional overlap between the distribution of labeled neurotensin binding sites and that of intense acetylcholinesterase staining in all of the above regions, except in the bed nucleus of the stria terminalis, claustrum, and central amygdaloid nucleus, where dense 125I-neurotensin labeling was detected over areas containing only weak to moderate cholinesterase staining. At higher magnification, 125I-neurotensin-labeled binding sites in the islands of Calleja, supraoptic nucleus of the hypothalamus, medial septum, diagonal band nucleus, and nucleus basalis of Meynert were selectively associated with neuronal perikarya found to be cholinesterase-positive in adjacent sections. Moderate 125I-neurotensin binding was also apparent over the cholinesterase-reactive neuropil of these latter three regions. These data suggest that neurotensin (NT) may directly influence the activity of magnocellular cholinergic neurons in the human basal forebrain, and may be involved in the physiopathology of dementing disorders such as Alzheimer's disease, in which these neurons have been shown to be affected.
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PMID:Distribution of 125I-neurotensin binding sites in human forebrain: comparison with the localization of acetylcholinesterase. 216 57

Adult male Long-Evans rats were injected intraperitoneally with 1.5, 3.0 or 9.0 micrograms/kg of anatoxin-a(s) that had been extracted from laboratory-grown Anabaena flos-aquae NRC-525-17, 800 micrograms/kg of paraoxon, or a control solution. Blood, anterior spinal cord, and brain cerebellar, cortical, medullary, midbrain, hippocampal, hypothalamic, olfactory and striatal cholinesterase activity was determined in rats that died prior to 2 hours or were anesthetized and killed at 2 hours. Unlike paraoxon, anatoxin-a(s) did not cause detectable inhibition of cholinesterase in the central nervous system, but did cause inhibition of cholinesterase in blood, suggesting that anatoxin-a(s) is strictly a peripheral cholinesterase inhibitor.
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PMID:Regional brain cholinesterase activity in rats injected intraperitoneally with anatoxin-a(s) or paraoxon. 281 13

Inhibition of central nervous system cholinesterase with a single pulse of physostigmine induces a pronounced increase of blood flow in the neocortex, cingulate gyrus, claustrum, and amygdala. This phenomenon is not accompanied by an increase in energy metabolism and may help explain the effect of this drug on memory in normal humans and patients with Alzheimer's disease, as well as other conditions. In contrast, a parallel increase of blood flow and metabolism was observed in the superior colliculus, a component of the visual pathways. Prolonged administration of physostigmine lead to persistent vasodilatation in the neocortex, a lessening of this effect in cingulate gyrus, claustrum and amygdala, and an increase in primary olfactory cortex and hippocampus when compared with single pulse administration. Effects of physostigmine on glucose utilization remained essentially the same as with pulse administration.
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PMID:Physostigmine enhances blood flow-metabolism ratio in neocortex. 315 Aug 7

In the olfactory bulb of Rana temporaria the distribution of cholinesterase was studied by the method of Karnovsky and Roots. When the butyrilthiocholine was used as a substrate the histochemical reaction was not obtained. The incubation with the acetylthiocholine showed the enzyme activity that was most pronounced in the mitral cells layer and in the nerve fibers area surrounding the granular cells layer. The addition of neostigmine to the incubation medium abolished the enzyme activity.
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PMID:[Histochemical study of the cholinesterase in the olfactory bulb of the frog, Rana temporaria]. 697 Apr 73

A comparative study of six hydrolases, acid and alkaline phosphatases, aryl sulphatase, beta-glucuronidase cholinesterase, and non-specific esterase, was carried out on the tissues of normal healthy and Frescon-treated Bulinus. The presence and activity of these enzymes in the tissues of normal animals were taken to indicate the probable functions of the tissues concerned. Frescon administration caused inhibition of acid phosphatase and also induced the release of cholinesterase and non-specific esterase in some tissues. It is concluded that the most important effects of Frescon on snail physiology are the disorganization of neuronal function and disturbance of olfactory activity.
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PMID:Histochemical studies of some enzymes in the tissues of the schistosome vector snail Bulinus truncatus (audouin) with special reference to the effects of a molluscicide. II. Hydrolases. 745 Dec 41

The effects of olfactory bulbectomy on the learning and memory of rats were examined, using several memory tasks. In reference memory and working memory tasks using a 3-panel runway apparatus, acquisition was delayed markedly by bilateral ablation of the olfactory bulb (OB). OB lesion performed after acquisition markedly impaired both reference and working memories. Even when the tasks were repeated for several sessions, the impairment of memory in OB-lesioned rats did not recover to the control level of the sham operation group. The delayed matching-to-lever location (DMLL) performance, which was examined using a 3-lever operant apparatus, was markedly impaired by OB lesions. This impairment was mild immediately after surgery, but tended to increase with time. Rats with OB-olfactory tubercule lesions show more severe impairment of memory in the DMLL performance. Reversal learning, using a 2-lever operant apparatus, was markedly impaired by OB lesions. The impairment of working and reference memories in OB lesioned rats, which was assessed using a 3-panel-runway apparatus, was reduced by cholinesterase inhibitor physostigmine and NIK-247. These findings suggest that the OB plays a very important role in the learning and memory processes necessary for both a working memory task and a reference memory task and that, at least in part, the memory impairment in OB lesioned rats is mediated by lowering of cholinergic function.
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PMID:Olfactory bulbectomy leads to learning/memory impairments in 3-panel runway and 3-lever operant tasks. 797 32

Soman (pinacolymethylphosphonofluoridate), a highly potent, irreversible inhibitor of cholinesterase, causes intense convulsions, neuropathology and, ultimately, death. There is evidence that certain brain structures are selectively vulnerable to the pathological consequences of soman-induced seizures. A working hypothesis is that central nervous system (CNS) structures with the earliest and most severe signs of neuropathology may be key sites for the initiation of the seizures. Fos, the immediate-early gene product, increases rapidly in several animal seizure models. Thus, we reasoned that the earliest brain regions to express Fos might be involved in the initiation and maintenance of soman-induced convulsions. To assess this, rats were injected with a single, convulsive dose of soman (77.7 micrograms/kg, i.m.). The animals were euthanized and processed for immunocytochemical analysis at several time points. Robust Fos expression was seen in layer II of the piriform cortex and the noradrenergic nucleus locus coeruleus within 30-45 minutes. One hour following soman injection, staining was more intense in the piriform cortex layer II and in the locus coeruleus. In addition, Fos was evident in the piriform cortex layer III, the entorhinal cortex, the endopiriform nucleus, the olfactory tubercle, the anterior olfactory nucleus and the main olfactory bulb. By 2 hours, Fos staining was present throughout the cerebral cortex, thalamus, caudate-putamen and the hippocampus. At 8 hours and beyond, Fos expression returned to control levels throughout the CNS except for the piriform cortex and the locus coeruleus which still had robust labeling. By 24 hours, neuropathology was evident throughout the rostral-caudal extent of layer II of the piriform cortex. The rapid induction of Fos in the piriform cortex and the locus coeruleus, taken together with previous anatomical, eletrophysiological and neurochemical studies, suggests that prolonged, excessive exposure to synaptically released acetylcholine and norepinephrine triggers the production of soman-induced seizures initially in the piriform cortex and subsequently in other cortical and subcortical structures.
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PMID:Anatomical localization and time course of Fos expression following soman-induced seizures. 903 4

Chronic, low-level exposure to cholinesterase inhibitor organophosphate (OP) insecticides or chemical warfare agents produces abnormalities in CNS acetylcholine (ACh) function, and in humans, may be associated with impaired cognitive function as well after withdrawal from such exposure. The purpose of the present study was to identify the severity of impairment in spatial learning of rats following protracted withdrawal from chronic, low-level exposure to the OP agent diisopropylfluorophosphate (DFP). Assessment of spatial learning began either 3 or 17 days after completion of a 14-day DFP treatment regimen (50, 250, or 500 micrograms/kg). During the 14-day treatment regimen, spontaneous activity and olfactory behaviors were suppressed, effects which subsided with repeated exposure to the 250 micrograms/kg dose regimen. In contrast, both behaviors were stimulated by exposure to the 50 micrograms/kg dose regimen, as was body weight gain. Performance of the spatial test of working memory was impaired for up to 21 days after withdrawal from treatment with a 250 micrograms/kg dose of DFP. AChE activity in the frontal cortex and hippocampus was suppressed to 42.58% and 50.35% of control levels, respectively, 3 days after completion of the DFP (250 micrograms/kg) treatment regimen. By 7 days after withdrawal from treatment, AChE activity in the cortex and hippocampus had recovered to 81.87% and 64.61% of control levels, respectively. These levels represent increases in activity of 39.29% and 14.26% in these regions, as compared to AChE activity in 3 days after DFP withdrawal. By 21 days after withdrawal from treatment, AChE in both brain regions had recovered to levels similar to those of controls. Chronic, low-level OP exposure, therefore, produces protracted impairment of working memory after drug withdrawal that is not associated with continued suppression of AChE activity. This impairment may, however, be associated with a decreased rate of AChE recovery in the hippocampus, relative to the cortex. This decreased rate of enzyme recovery may contribute to hippocampal toxicity underlying protracted impairment of working memory.
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PMID:Chronic, low-level exposure to diisopropylfluorophosphate causes protracted impairment of spatial navigation learning. 904 Jan 25

The memory impairment of olfactory bulbs (OB)-lesioned rats was characterized using 4 different tasks of learning/memory, and the effects of certain cholinergic drugs on such memory impairment were examined. In reference memory and working memory tasks using a 3-panel runway apparatus, OB-lesioned rats showed a marked increase in errors. In the 3-lever operant task using delayed matching to a sample (DMTS) procedure, OB lesions significantly decreased the correct response in choice (test) trials without affecting the in sample (training) trials. An interesting finding is that impairment in the DMTS performance did not appear immediately after the OB lesion, but tended to appear after a delay. Based on this finding, it is unlikely that memory impairment in the OB-lesioned rats is due to the olfactory deficit itself. However, OB lesions significantly reduced the choice accuracy and delayed the choice reaction time during the 3-choice serial time task for assessing attentional function, using a 3-lever operant apparatus. These findings suggest that marked impairment of learning and memory in OB-lesioned rats may be caused by the attention deficit. Furthermore, the memory impairment in OB-lesioned rats was reduced by cholinesterase inhibitors, physostigmine and NIK-247. These finding suggest that dysfunction of the cholinergic system is involved, at least in part, in the memory impairment of OB-lesioned rats.
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PMID:Characteristics of memory dysfunction in olfactory bulbectomized rats and the effects of cholinergic drugs. 906 61


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