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)

The distribution of dihydronicotinamide adenine dinucleotide phosphate diaphorase (NADPH diaphorase) was studied by enzyme histochemistry in the striatum of the adult cat. Neurons and neuropil expressing NADPH diaphorase activity were found throughout the striatum. The diaphorase-positive neurons formed a sparse population of medium-sized cells. In the caudate nucleus they were recognized by antisera against somatostatin 14, somatostatin 28(1-12), neuropeptide Y and avian pancreatic polypeptide. The diaphorase activity of the striatal neuropil was characterized by a modular organization that was particularly distinct in the caudate nucleus. This organization was analyzed by comparing the patterns of diaphorase staining with the distribution of acetylcholinesterase activity in adjacent sections. The NADPH diaphorase activity was found to be dense in the acetylcholinesterase-rich matrix of the caudate nucleus, but weak in the acetylcholinesterase-poor compartments known as striosomes. Because of the colocalization of perikaryal NADPH diaphorase activity and somatostatinlike immunoreactivity, a comparison was also made between the distribution of diaphorase staining and immunostaining for somatostatinlike peptide in the striatal neuropil. Both observed striosomal ordering, so that the acetylcholinesterase-poor zones detected in adjoining sections corresponded to regions of low somatostatinlike immunoreactivity as well as low NADPH diaphorase staining. In some regions striosomes were more clearly delineated in the stains for diaphorase and somatostatinlike suggest that NADPH diaphorase may be a sensitive marker for the somatostatinergic neuropil as well as the somatostatinergic perikarya of the striatum, and that this enzyme could prove valuable in attempts to differentiate the processes of intrinsic somatostatin-containing fibers from any extrinsic somatostatin afferents that may exist.
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PMID:A new enzyme marker for striatal compartmentalization: NADPH diaphorase activity in the caudate nucleus and putamen of the cat. 241 68

Neurons expressing immunoreactivity to antisera against somatostatin 14 and other somatostatin-related peptides were identified in the striatum of cats and nonhuman primates. In each species, immunoreactive neurons were distributed singly and in small groups in the caudate nucleus, putamen and ventral striatum. A detailed study was made of somatostatin-positive neurons and neuropil in the caudate nucleus of the cat. First, the mean diameters and surface areas of neurons expressing immunoreactivity to somatostatin 14 were made from peroxidase-antiperoxidase stained material. Second, fluorescence immunohistochemistry was combined with retrograde labeling of striatal neurons to determine whether such somatostatin 14-positive neurons emit axons projecting out of the striatum. Third, the distributions of neurons and neuropil expressing immunoreactivity to somatostatin 14 or somatostatin 28 (1-12) were plotted in relation to the locations of acetylcholinesterase-poor zones ("striosomes") visible in adjoining sections. The morphometric analysis suggested that somatostatin 14-positive neurons in the caudate nucleus form a single population of medium to medium-large neurons having mean diameters of 20 micron and mean surface areas of 154 micron2. The retrograde tracer study suggested that these somatostatin 14-positive neurons are interneurons. Injections of fast blue into all of the known targets of striatofugal fiber projections failed to label somatostatin 14-positive neurons save in a few instances (less than 0.3% of more than 4000 neurons) in each of which labeling was equivocal. Analysis of the distribution of somatostatin-positive neurons and neuropil in the striatum demonstrated that both observe striosomal ordering. Somatostatin immunoreactive neuropil was dense outside and weak inside identified striosomes, and most immunoreactive neurons lay outside. Often somatostatin-positive neurons lay beside, and sometimes striosomes partly rimmed them. The processes of such neurons tended to run along the borders of the striosomes without crossing them, but occasionally single processes and rarely entire dendritic trees crossed from one compartment to the other. These results suggest that, in the striatum of the cat, somatostatin is present: (1) in fibers organized according to the compartmental distribution already recognized for other neurochemical compounds in the striatum as well as for its afferent and efferent systems, and (2) in interneurons, mostly present in the extrastriosomal matrix, but also located near striosomes, where they could serve as interfaces between the striosomes and extrastriosomal matrix.
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PMID:Striatal neurons expressing somatostatin-like immunoreactivity: evidence for a peptidergic interneuronal system in the cat. 242 90

The frequency of occurrence of the adrenergic, cholinergic, 5-hydroxytryptamine (5-HT)-, substance P (SP)-, methionine-enkephalin (met-Enk)- and somatostatin (SOM)-immunoreactive fibres innervating the smooth muscle of the large intestine in Hirschsprung and control children was compared. It was observed a higher frequency of catecholamine-fluorescence, acetylcholinesterase-positive and SOM-immunoreactive fibres in the muscularis externa and muscularis mucosa of the aganglionic segment in Hirschsprung gut as compared to that in the sigmoid colon and rectum in controls. In contrast, the frequency of SP-, met-Enk- and 5-HT-immunoreactive fibres in the aganglionic segment in Hirschsprung gut was lower than that in the controls. Ultrastructurally the cholinergic and adrenergic fibres occurred more often in the aganglionic segment in Hirschsprung gut than in the controls. A treatment with 6-OHDA and a fixation by Tranzer and Richards technique was used to confirm the nature of the adrenergic fibres. The p-type fibres occurred infrequently in the aganglionic segment of Hirschsprung gut. The results suggest that the change in the frequency of the nerves containing inhibitory transmitters may play an important role in the pathogenesis of Hirschsprung's disease.
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PMID:Histochemical, immunocytochemical and ultrastructural data on the innervation of the smooth muscle of the large intestine in Hirschsprung's disease. 242 97

Acetylcholinesterase, somatostatin-like immunoreactivity, and homovanillic acid levels were measured in the cerebrospinal fluid of 36 patients with early stages of Parkinson's disease and in 19 control patients. In patients with Parkinson's disease the levels of somatostatin-like immunoreactivity were lower than in the controls (p less than 0.01); these values were lowest in the demented Parkinsonian patients. Concentrations of homovanillic acid were also significantly lower in Parkinsonian patients (p less than 0.05). In contrast, no changes were observed in the acetylcholinesterase activity of patients with Parkinson's disease. The reduced somatostatin-like immunoreactivity in CSF agrees with previous post-mortem studies and indicates that Parkinson's disease and Alzheimer's disease may have some neurochemical features in common.
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PMID:Somatostatin-like immunoreactivity in the cerebrospinal fluid of patients with Parkinson's disease and its relation to dementia. 243 3

Monoamine metabolites, biopterin, acetylcholinesterase (AChE) activity, and somatostatin-like immunoreactivity (SLI) were determined in the lumbar cerebrospinal fluid (CSF) of 24 patients with dementia of the Alzheimer type (DAT) without myoclonus or extrapyramidal signs, in 8 patients with DAT and myoclonus, and in 14 age-matched healthy control subjects. In patients with DAT with myoclonus as compared with both DAT patients without myoclonus and control subjects, the concentrations of homovanillic acid and biopterin were significantly decreased. 5-Hydroxyindoleacetic acid was significantly lower in patients with myoclonic DAT as compared to patients with nonmyoclonic DAT, but not significantly lower than in control subjects. CSF AChE and SLI were significantly reduced in patients with DAT with or without myoclonus, as compared with control subjects, but AChE and SLI were not significantly different between dementia groups. These results suggest that DAT patients with myoclonus represent a distinct clinical and neurochemical DAT subtype.
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PMID:Cerebrospinal fluid neurochemistry in the myoclonic subtype of Alzheimer's disease. 246 3

Fetal striatal grafts display a striking modularity of composition. With acetylcholinesterase (AChE) histochemistry, the tissue of such grafts can be divided into regions with strong AChE staining of the neuropil and regions in which AChE staining of the neuropil is weak. In the experiments reported here, we reexamined the nature of this modularity. Striatal grafts were made by injecting dissociated cells of E15 ganglionic eminence into the striatum of adult rats, which 7 days before had recived intrastriatal deposits of ibotenic acid. Some donors had been exposed to 3H-thymidine at E11-E15. After 9-17 month survivals, the anatomical organization of the grafts was studied by histochemistry, immunohistochemistry, and autoradiography. In every graft, the AChE-rich regions formed patches (P regions) in a larger AChE-poor surround (NP regions). Neurons labeled with 3H-thymidine appeared in both P and NP regions, suggesting that donor cells were distributed in each type of region and that neither type of tissue, P or NP, was composed exclusively of host tissue. In the AChE-rich P regions, markers characteristic of normal perinatal and mature rat striatum were expressed by medium-sized cells: calcium-binding protein (calbindin D28k) immunostaining, metenkephalin (mENK) immunostaining, and, more rarely, somatostatin (SOM) immunostaining. In the NP regions, however, medium-sized cells expressing calbindin and mENK immunostaining were very rare, and there was an abundance of neuronal types not found in normal mature striatal tissue. These included (1) large, multipolar, calbindin-positive neurons with well-ramified, densely stained dendrites, (2) large, SOM-positive neurons with prominent dendritic trees, and (3) mENK-positive cells smaller than typical striatal, medium-sized, mENK-immunoreactive neurons. In Nissl stains, the AChE-rich P regions resembled the normal striatum of mature animals, whereas the AChE-poor NP regions did not. These findings suggest that the P regions of fetal striatal grafts achieve a phenotypy similar to that of normal striatum at maturity and during much of postnatal development. The dominant expression of perikaryal calbindin-like immunoreactivity in the P regions further suggests that these zones have a high proportion of tissue resembling striatal matrix. By contrast, expression of marker antigens in the NP zones of the grafts suggests that these zones are predominantly composed of nonstriatal tissue or that they have the phenotypy of immature striatum intermixed with some nonstriatal cells.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Intrastriatal grafts derived from fetal striatal primordia. I. Phenotypy and modular organization. 247 13

In obesity the reduced growth hormone (GH) responses to several provocative stimuli including growth hormone-releasing hormone (GHRH) indicate a diminished somatotroph responsiveness but do not distinguish between primary pituitary and hypothalamic pathogenesis. However, it has been shown that the cholinergic system positively influences Gh secretion likely by modulating somatostatin release in a negative way. Thus, the effect of cholinergic activity enhancement by pyridostigmine (PD), an acetylcholinesterase inhibitor, on both basal and GHRH-induced GH secretion was studied in 14 obese subjects (eight adults and six children). Eighteen nonobese subjects (seven adults and 11 children) were studied as controls. In obese subjects the GHRH-induced GH increase was lower than in controls (peak, mean +/- SEM, adults, 9.2 +/- 2.7 v 16.8 +/- 5.7 ng/mL; children, 8.0 +/- 0.8 v 20.3 +/- 4.6 ng/mL) attaining statistical significance only in children group (P less than .02). The PD-induced GH response in the two obese groups was similar to that observed in relative controls (adults, 5.3 +/- 1.0 v 7.4 +/- 1.7 ng/mL; children, 9.6 +/- 1.6 v 13.3 +/- 1.4 ng/mL). PD clearly potentiated the GH response to GHRH in obese subjects, both adults (P less than .05 v GHRH alone) and children (P less than .0005 v GHRH alone). However, the GH responses to PD + GHRH was significantly reduced in obese subjects compared with controls (adults, 18.1 +/- 2.2 v 42.7 +/- 10.7 ng/mL, P less than .05; children, 28.3 +/- 4.5 v 58.2 +/- 7.7 ng/mL, P less than .01). In conclusion, PD is able to potentiate the blunted GH responses to GHRH in obese adults and children, inducing a GH increase similar to that observed after GHRH alone in normal subjects. This finding suggests that an alteration of somatostatinergic tone could be involved in the reduced GH secretion in obesity.
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PMID:Effect of cholinergic enhancement by pyridostigmine on growth hormone secretion in obese adults and children. 250 May 77

In man the GH response to GHRH is highly variable and some normal subjects may be completely unresponsive to the neuropeptide. On the other hand, the potentiation of cholinergic activity by pyridostigmine (PD), a cholinesterase inhibitor, increases the GH response to GHRH, probably by inhibiting somatostatin release. The aim of this study was to assess the existence of intraindividual variability in the GH response to GHRH and verify the effects of PD treatment on inter- and intraindividual variability. Twenty normal adults (17 M and 3 F) and 10 normal prepubertal children (9 M and 1 F) underwent 2-5 administrations of 1 micrograms/kg GHRH on different days. Seven adults and all children also underwent 1-5 other tests in which GHRH was preceded (60 min before) by oral PD (120 mg in adults and 60 mg in children). The GH responses to GHRH were highly variable, not only within subjects but also in the same subject on different occasions (peak range; adults: 0.4-49.0 ng/ml; children: 2.4-50.0 ng/ml). PD always markedly increased the GH response to GHRH, even unmasking this response in 3 adults and 4 children hyporesponsive to the neuropeptide alone. However, the variability in the GH response was still present (adults: 27.2-108.5 ng/ml; children: 25.0-144.0 ng/ml), though reduced (adults: p = 0.0005; children: p = 0.0204). These data indicate that: i. A great inter- and intraindividual variability in the GH response to GHRH is present.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of the potentiation of cholinergic activity on the variability in individual GH response to GH-releasing hormone. 251 19

Acute hyperglycemia blocks growth hormone (GH) secretion in response to provocative stimuli including growth hormone releasing hormone (GHRH) administration. However, the precise mechanism of glucose action is unknown. To determine if enhanced somatostatinergic stimulation accounts for the decreased GH secretion, we studied the effect of enhanced cholinergic tone by pyridostigmine on the hyperglycemia blockade of GH release in 7 normal subjects. Pyridostigmine, an acetylcholinesterase inhibitor, has been postulated as an inhibitor of somatostatin release. Each subject underwent 4 tests with GHRH injection (100 micrograms i.v. at 0 min). In the first (control) test, placebo was administered before GHRH. In the second test, 100 g of glucose was administered p.o. 45 min before GHRH. In the third test, pyridostigmine, 120 mg p.o., was administered 60 min before GHRH, and in the fourth test, pyridostigmine, glucose and GHRH were administered at -60, -45 and 0 min, respectively. GHRH-induced GH secretion of 25.8 +/- 4.5 ng/ml was significantly reduced by previous glucose administration (12.1 +/- 4.5 ng/ml) and significantly potentiated by previous pyridostigmine pretreatment (56.5 +/- 16.8 ng/ml). In the fourth test (pyridostigmine plus glucose plus GHRH) the GH peak of 42.4 +/- 9.2 ng/ml was significantly higher than after GHRH alone and not different to the pyridostigmine-GHRH test. In conclusion, central cholinergic activation by pyridostigmine reversed the hyperglycemic blockade of GHRH-induced GH secretion. In addition, hyperglycemia was unable to reduce the potentiating effect of pyridostigmine on GH secretion elicited by GHRH. Based on the reported actions of pyridostigmine, acute hyperglycemia might act over GH release by inducing hypothalamic somatostatin release.
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PMID:Activation of cholinergic neurotransmission by pyridostigmine reverses the inhibitory effect of hyperglycemia on growth hormone (GH) releasing hormone-induced GH secretion in man: does acute hyperglycemia act through hypothalamic release of somatostatin? 256 42

Through an epidemiological survey, we observed 3 types of clinical courses among patients with senile dementia of the Alzheimer type (SDAT). The mental ability of the patients declined rapidly (Group A; n = 11), gradually (Group B; n = 6), or showed extremely slow changes (Group C; n = 9). The acetylcholinesterase (AChE) activity and somatostatin (SRIF) concentration of the cerebrospinal fluid (CSF) were measured in patients with Alzheimer's disease (AD) and 3 types of SDAT. Both AChE activity and SRIF concentration of CSF were significantly lower in Group A and among patients with AD compared with age-matched control subjects. Both AChE activity and SRIF concentration of CSF were not significantly different in Groups B and C. This biochemical study confirmed our epidemiological finding that only the patients in Group A with SDAT closely resembled the clinical course of AD and may belong to the category of neurodegenerative disorders.
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PMID:Characterization of the course of senile dementia of the Alzheimer type using cerebrospinal fluid levels of acetylcholinesterase and somatostatin. 257 39


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