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)

Enzyme immunoassays (EIAs) for Thyroliberin (TRH) and TRH-elongated peptides were developed. Three haptens less than E-H-P-NH2 (TRH). Less than E-H-P-OH (TRH-OH), and S-K-R-Q-H-P-G-K-R-F (P10) were conjugated by the use of different heterobifunctional cross-linking agents either to sun-flower globulin as carrier or to acetylcholinesterase as tracer. For a same hapten, the same chemical group in the peptide was used to prepare the immunogen and the enzyme conjugate. These EIAs were performed with a second antibody solid phase technique using acetylcholinesterase as label. They permitted the measurement of TRH and TRH-elongated peptides with a sensitivity threshold of 10 fmol/well for TRH and 2 fmol/well for P10. TRH EIA only detected authentic TRH whereas TRH-OH EIA detected TRH and TRH peptides elongated on C terminal part. Anti-P10 serum was specific of TRH peptides elongated both on C and N terminal parts and no cross reactivity was observed with TRH. Using these assays, TRH and TRH-elongated peptides were determined in crude or chromatographed mouse and rat hypothalamus tissular extracts. Several TRH extended forms were identified by P10 EIA, whereas TRH-OH EIA permitted detection of both TRH and TRH-elongated peptides in chromatographed extracts. Authentic TRH was measured by TRH EIA both in crude and chromatographed hypothalamic extracts. These assays can permit the study of the processing and maturation of TRH.
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PMID:Enzyme immunoassays for thyroliberin (TRH) and TRH-elongated peptides in mouse and rat hypothalamus. 212 11

The rat cerebellar cortex is built from parasagittally arranged modules with topographically ordered afferent and efferent projections. The intrinsic organization of the cerebellum is revealed by immunocytochemical staining with monoclonal antibody, mabQ113. In the cerebellum, mabQ113 recognizes a polypeptide epitope that is restricted to a subset of Purkinje cells. Antigenic Purkinje cells are clustered to form a complex pattern of parasagittal compartments. Several biochemical markers reveal a superficially similar organization of the cortex, and so it is important to determine how many independent maps are present. This report compares the mabQ113 antigen display to the patchy distribution of acetylcholinesterase (AChE). In the granular layer and the white matter of the adult cerebellar cortex there is a patchy AChE staining that includes both the hemispheres and the vermis. The staining is often not sharply resolved cytologically, but seems to be associated primarily with the synaptic glomeruli. The boundaries of these granular layer patches in the vermis correspond to the mabQ113+/mabQ113- boundaries of the overlying Purkinje cell compartments. Thus, AChE and mabQ113 antigen share a common compartmentation both in the vermis, and in the hemispheres. Both mabQ113 and AChE distributions develop postnatally in the cerebellar cortex. At birth (PO) there is neither AChE activity nor mabQ113 immunoreactivity. Both staining patterns emerge during the second postnatal week. In the vermis at P10, there is AChE activity in the granular layer and white matter, and the distribution is already patchy despite the absence of synaptic glomeruli. At the same age the mabQ113 immunoreactivity is found in all Purkinje cells rather than a subset, and the band pattern has yet to mature. There is also transient AChE staining of Purkinje cell somata and dendrites. The AChE patches clarify between P10 and P20 along with the appearance of the synaptic glomeruli and the development of differential mabQ113 staining, but there is no reason to believe that the two are causally linked. In contrast to the cerebellar cortex, AChE staining in the cerebellar nuclei matures very early and at P0 the activity is already high. Zones of high and low AChE activity are seen in all the cerebellar nuclei and may be related to the distribution of the terminal fields of the different Purkinje cell populations.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Zonation in the rat cerebellar cortex: patches of high acetylcholinesterase activity in the granular layer are congruent with Purkinje cell compartments. 325 99

Histochemical techniques have been used to examine the development of the enzyme acetylcholinesterase (AChE) in normal and transplanted rat superior colliculus (SC). At birth (P0), relatively little AChE activity was found in SC in situ; however, there was a gradual increase in the intensity of AChE staining in the SC over the first 4 postnatal weeks. In the superficial layers, an increase in AChE activity was first seen in rostromedial SC at P6 and was found throughout the upper tectal layers by P10. An increase in AChE activity in the intermediate layers was apparent by P12 and the adult pattern, characterized by periodic bands of AChE staining, was established by P22. In tectal grafts, the development of AChE activity followed a time course similar to that found in normal SC. Mature tectal grafts contained moderate AChE activity with AChE-positive cells scattered throughout the neuropil. There were however, localized, often spherically shaped areas which displayed relatively intense AChE activity. These AChE-dense areas had a characteristic appearance in adjacent sections stained for Nissl or neurofibrils. Significantly, host retinal input, where present, was always restricted to the AChE-dense regions and it seems certain that these areas are homologous to the superficial layers of normal SC. AChE-rich regions were also present, however, in grafts which received no retinal input and in general the pattern of AChE activity in tectal grafts was strikingly similar, irrespective of their location or connections with the host brain. It would appear, therefore, that much of the AChE activity in tectal transplants, and presumably in SC in situ, is intrinsic to that region and not derived from or dependent upon extrinsic innervation.
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PMID:The development of acetylcholinesterase activity in normal and transplanted superior colliculus in rats. 405 6

The development of acetylcholinesterase (AChE) activity within cortical neurons of the rat brain was investigated using a histochemical method. The fate of these neurons in later stages of development was studied in animals in which AChE within cortical axons (mostly cholinergic) had been depleted by lesions of the cholinergic neurons of the basal forebrain or by injections of diisopropyl fluorophosphate. We designated neurons with medium to high intensity of reaction product as AChEH and neurons with a low intensity of reaction product as AChEL. Four groups of AChEH cortical neurons were detected: (1) AChEH Cajal-Retzius cells were present in layer I at birth (P0) and decreased steadily in number until none could be detected at P17 or thereafter. (2) AChEH neurons within layer VI and underlying white matter were present at P0, peaked in number and staining intensity at P8-P9, showed a moderate decrease in number at P11-P13 and a further decrease into adulthood. (3) AChEH polymorphic intracortical neurons appeared at P3-P4 in deep cortical layers and by P9 were present in layers II-VI. They continued to increase in number through P11-P14 at which time they displayed the adult pattern and were found in all cortical areas. (4) A large population of AChEH pyramidal neurons appeared at P1-P4, peaked at P8-P10 and was no longer visible at P21. In the adult cerebral cortex, few pyramidal neurons displayed AChE activity and these were almost always of the AChEL type. These results indicate that the AChE within cortical neurons is developmentally regulated and that the content of this enzyme helps to differentiate cortical neurons into distinct populations. The transient expression of AChE activity within cortical neurons suggests a role for this enzyme in the development of the cerebral cortex.
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PMID:Postnatal development of cortical acetylcholinesterase-rich neurons in the rat brain: permanent and transient patterns. 755 36

Homozygote wobbler mice develop motoneurone degeneration. Throughout development the expression of choline acetyltransferase, of trkC receptor and F3 adhesion molecule genes is similar in wobbler and wild-type spinal cord. Acetylcholinesterase mRNA level instead is decreased to about 50% with respect to wild-type values in one forth of P5 and P10 wobbler progeny, putative wr/wr individuals; at P21 its expression is equally highly reduced in known homozygotes and it is reduced to 35% of normal values in about one half of the progeny, putative heterozygotes. Thus, similarly to medium neurofilament gene over-expression, reduced acetylcholinesterase gene expression is an early molecular marker for the wobbler mutation before onset of the illness.
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PMID:Acetylcholine esterase and peripherin mRNA level decrease in wobbler mouse. 760 8

Using a histochemical method for the visualization of cholinesterase activity in neurons, we have observed developmentally transient expression of acetylcholinesterase (AChE) in cortical pyramidal neurons of the rat brain. Depending on the extent of the deposition of AChE reaction product, several types of cortical neurons could be visualized. We designated neurons with moderate-to-high staining intensity as AChEH and neurons with relatively lower staining intensity as AChEL. At birth (P0), very little AChE activity was found within cortical neurons. Between P1-P4, there was a gradual emergence of AChE-stained cortical neurons. At this stage, the majority of these neurons were of the AChEL type. At P5-P7 we observed an abrupt increase in AChE-stained cortical neurons. The number and the staining intensity of these neurons was at a peak at P8-P10. At this age range, the majority of these neurons were of the AChEH variety and displayed morphological characteristics of cortical pyramidal neurons. At P11-P15, there was an abrupt decrease in the number of AChEH neurons. After P15, the density and staining intensity of cortical AChE-positive (cholinergic) axons gradually increased. Nevertheless, AChEL pyramidal neurons were detected through these fibers up to P21. At P21, a dense plexus of AChE-positive axons was observed in all cortical areas while very little AChE reaction product was visible in pyramidal neurons, and this pattern continued into adult life. When the adult cortex was denervated from its AChE-positive axons by lesions of the nucleus basalis magnocellularis, many AChEL pyramidal neurons were uncovered.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Developmentally transient expression of acetylcholinesterase within cortical pyramidal neurons of the rat brain. 830 28

We tested the effects of the acetylcholinesterase inhibitor eserine (10 microM), an indicator of the activity of endogenous ACh, on the generation of epileptiform discharges during blockade of inhibitory GABA(A)-mediated potentials by bicuculline (10 microM), in the CA3 area of hippocampal slices from postnatal days 4-20 (P4-P20) immature and adult rats. Eserine provoked or significantly increased the frequency of spontaneous synchronous epileptiform discharges, in 6/22 (27%) P4-P10 slices, 34/35 P11-P20 slices and 18/18 adult slices, an epileptogenic effect. In immature slices, spontaneous discharges showed a stable frequency throughout perfusion with eserine, while in 5/11 adult slices an initial fast frequency was followed by a slower steady-state one. The cholinergic agonist carbachol (CCh, 25 microM) provoked only transient or no spontaneous synchronous discharges in adult slices (n=8), thus suggesting that massive activation of cholinergic receptors may lead to suppression of epileptiform activity in adult brain. Stimulus-induced excitatory CA3 responses, were depressed by eserine in approximately half of 20 P4-P10, 45 P11-P20 and 11 adult slices. The depression consisted of a decrease in the amplitude, duration, and number of population spikes of the field potentials by about 30%, a minor neuroprotective effect, which did not change with maturation. The different developmental profiles of the epileptogenic and neuroprotective effects of endogenous ACh suggest that they are mediated by different mechanisms. These experiments demonstrate that, endogenous ACh is sufficient to induce epileptogenesis during a decrease or failure of GABAergic inhibition, in both >/=P10 immature and in adult hippocampus. We therefore suggest that clinical or behavioral conditions which raise the concentration of endogenous ACh may lower the threshold to seizures.
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PMID:Epileptiform activity generated by endogenous acetylcholine during blockade of GABAergic inhibition in immature and adult rat hippocampus. 1041 85

The distribution of acetylcholinesterase histochemistry and choline-O-acetyltransferase immunohistochemistry in the basal forebrain was studied in newborn mice (P0) and until 60 days of postnatal life (P60). A weak acetylcholinesterase activity was found at P0 and P2 in the anterior and intermediate parts of the basal forebrain, and higher in the posterior region. The intensity of labeling, neuronal size and dendritic growth seems to increase progressively in all regions of basal forebrain from P4 to P10. The AChE+ cell count shows that in the anterior portion of the magnocellular basal nucleus the number of cells does not vary significantly from birth to the second month of postnatal life. However, in the intermediate and posterior portions of the nucleus the mean number of labeled cells increases significantly from birth to the end of the second week of postnatal life (P13). The choline-acetyltransferase immunoreactivity appears only detectable at the end of the first week (P6) as a slight immunoreaction, which increases progressively in intensity at P8, and at P10 seems to attain the same intensity of labeling found at P60. These results seem to indicate that the acetylcholinesterase could have a non-classic cholinergic role in the first stages of postnatal development, acting as a growth and cellular differentiation factor.
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PMID:Postnatal development of cholinergic system in mouse basal forebrain: acetylcholinesterase histochemistry and choline-acetyltransferase immunoreactivity. 1147 Mar 79

Unlike the development of acetylcholinesterase (AChE) activity, the postnatal development of the activity of the related enzyme butyrylcholinesterase (BuChE) in the rodent brain has not been investigated in a comprehensive manner. The purpose of the present study was to fill this gap. Development of histochemically visualized BuChE activity followed four distinct stages. Between birth and five postnatal days (P0-P5) BuChE staining of very low intensity was present in nearly all neurons in the forebrain and upper brainstem. Substantial BuChE activity was present in the endothelial cells of blood vessels and the cuboidal cells lining the ventricles. At P6-P10, BuChE neuronal staining of high to moderate intensity emerged in many areas, including certain thalamic nuclei (e.g. anterior group), a number of brainstem nuclei, and darkly stained neurons in the olfactory tubercle/piriform cortex. At P11-P17, the staining which emerged in earlier stages was darker and had expanded to include more neurons. A scattered population of BuChE-positive neurons of moderate to high intensity emerged in the neocortex and amygdala. Importantly, at P17, the very light staining present in all neurons since birth was no longer visible. At P18-P30, the number and staining intensity of cortical neurons displayed a gradual increase while the staining in certain thalamic nuclei was substantially decreased or completely disappeared (e.g. ventral lateral nucleus). A prominent feature of this stage was the emergence of BuChE activity in many fiber tracts. At P30, the adult pattern of staining was attained. The transient presence of BuChE activity of very low intensity in all neurons and of higher intensity in thalamic neurons supports the implied role for this enzyme in neuronal development.
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PMID:Butyrylcholinesterase activity in the rat forebrain and upper brainstem: postnatal development and adult distribution. 1727 83

Acetylcholinesterase (AChE), a principal modulator of cholinergic neurotransmission, also has been demonstrated to be involved in the morphogenetic processes of neuronal and non-neuronal tissues. This study shows that AChE exhibits temporospatial activity in the dental epithelium of the developing mouse tooth. To identify the AChE activity in the mouse tooth during development, we performed enzyme histochemistry on the mouse embryos from embryonic day 13 (E13) to E18 and on the incisors and molars of the neonatal mouse at 10 days after birth (P10). In the developing molars of mouse embryos, AChE activity was not found in the dental epithelium at E13 (bud stage). AChE activity first appeared in the developing cervical loops of the enamel organ at E14 (cap stage), but was not found in the enamel knot. At E18 (bell stage), AChE activity was localized in the inner enamel epithelium except the cervical-loop area. In the incisors and molars of neonatal mice (P10), AChE activity was localized in the inner enamel epithelium of the cervical-loop and enamel-free area. Overall, AChE activity was localized in the differentiating dental epithelium while the activity of butyrylcholinesterse, another cholinesterase, was located primarily in the cells of the dental follicle. The results suggest that AChE may play a role in the histo- and cytodifferentiation of dental epithelium during tooth development.
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PMID:Temporospatial localization of acetylcholinesterase activity in the dental epithelium during mouse tooth development. 1790 11


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