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 expression of nerve growth factor receptor (NGFR) transcripts was investigated with in situ hybridization techniques in the CNS of chick embryos from 3 days of incubation (E3) to 14 days posthatch (P14). The time course and distribution of NGFR expression was compared with the development of the cholinergic phenotype. Cholinergic properties were assessed by immunolabeling for choline acetyltransferase (ChAT) and histochemistry for acetylcholinesterase (AchE) activity. NGFR transcripts are expressed transiently in the inner plexiform layer and ganglion cell layer of the retina (E4-P1), neostriatum and hippocampus (E18), infundibular hypothalamus (E7-18), spiriform complex (E9-15), layers 2, 3 (E9-18), and 10 (E11-18) of the optic tectum, nucleus mesencephalicus profundus, pars ventralis (E9-18), parvicellular isthmic nucleus (E7-P1), magnocellular isthmic nucleus (E9-E18), nucleus semilunaris (E7-18), isthmo-optic nucleus (E7-P14), rostral motor nuclei (E5-18), developing cerebellum (E7-15), internal granule cell layer (E11-18) and Purkinje cell layer (E15-P14) of the cerebellar cortex, and the inferior olivary nucleus (E9-15). A small number of neuronal populations with embryonic expression of NGFR remain strongly NGFR-positive in the posthatch animal:habenular nuclei (labeled after E5), nucleus subrotundus (after E9), mesencephalic trigeminal nucleus (after E5), caudal parts of locus ceruleus and nucleus subceruleus (after E7), medullar reticular nuclei (after E11), and motor nuclei IX, X, and XII (after E9). The majority of neuronal populations with NGFR expression show cholinergic properties in development, and NGFR expression always precedes the onset of ChAT immunoreactivity. Postnatal expression of growth factor receptors is largely confined to neurons of the reticular type. NGFR expression in avian CNS nuclei differs from that in mammals. Early loss of NGFR expression in the cholinergic basal forebrain (which remains strongly NGFR positive in mammals) and persistent NGFR expression in parts of the avian locus ceruleus indicate changes of growth factor receptor expression and growth factor requirements in phylogeny. Knowledge of the time and distribution of NGFR expression in the chick embryo will facilitate the assessment of specific functions of NGF and NGF-like molecules in an embryonic model with easy access for experimental manipulations.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Expression of nerve growth factor (NGF) receptors in the brain and retina of chick embryos: comparison with cholinergic development. 165 88

Experiments were done to study the fate of transient catecholaminergic (TC) cells that develop in the rodent gut during ontogeny. When they are first detected, at Day E11 in rats, TC cells are distributed along the vagal pathway, in advance of the descending fibers of the vagus nerves, and in the foregut. The early TC cells coexpress the immunoreactivities of several neural markers, including 150-kDa neurofilament protein, peripherin, microtubule associated protein (MAP) 5, and growth-associated protein (GAP)-43, with those of the catecholamine biosynthetic enzymes tyrosine hydroxylase (TH) and dopamine-beta-hydroxylase (DBH). All cells in the fetal rat bowel at Day E11 that express neural markers also express TH immunoreactivity. The primitive TC cells also express the immunoreactivities of neural cell adhesion molecule (N-CAM), neuropeptide Y (NPY), and nerve growth factor (NGF) receptor (and NGF receptor mRNA). By Day E12 TC cells are found along the vagal pathway and throughout the entire preumbilical bowel. At this age TC cells acquire additional characteristics, including MAP 2 and synaptophysin immunoreactivities and acetylcholinesterase activity, which indicate that they continue to mature as neurons. In addition, TC cells of the rat are immunostained at Day E12 by the NC-1 monoclonal antibody, which in rats labels multiple cell types including migrating cells of neural crest origin. Despite their neural properties, at least some TC cells divide and therefore are neural precursors and not terminally differentiated neurons. At Day E10 TH mRNA-containing cells were not detected by in situ hybridization; however, by Day E11 TH mRNA was detected in sympathetic ganglia and in scattered cells in the mesenchyme of the foregut and vagal pathway. At this age, the number of enteric and vagal cells containing TH mRNA is about 30% less than the number of cells containing TH immunoreactivity in adjacent sections. The ratio of TH mRNA-containing cells to TH-immunoreactive vagal and enteric cells is even less at Day E12, especially in more caudal regions of the preumbilical bowel. A similar decline in the ratio of TH mRNA-containing to TH-immunoreactive cells was not observed in sympathetic ganglia. After Day E12 TH mRNA cannot be detected in enteric or vagal cells by in situ hybridization; nevertheless, TH immunoreactivity continues to be present through Day E14. DBH, NPY, and NGF receptor immunoreactivities are expressed by TH-immunoreactive transitional cells in the fetal rat gut after TH mRNA is no longer detectable.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Transiently catecholaminergic (TC) cells in the bowel of the fetal rat: precursors of noncatecholaminergic enteric neurons. 197 56

Transient catecholaminergic (TC) cells have been found to appear in the vagal pathway and bowel of fetal mice and rats. It has been proposed that these cells are migrating vagal crest-derived precursors of enteric neurons that lose their catecholaminergic properties when they terminally differentiate. In the current experiments, segments of fetal mouse gut were explanted before (day E9) TC cells or any neural markers could be detected in situ. Tyrosine hydroxylase (TH)-immunoreactive neurons developed in vitro in 4/12 such explants; therefore, cells with a catecholaminergic potential are present in the gut of at least some animals prior to the in situ expression of this phenotype. The neurogenic potential of cells in the vagal pathway was similarly tested by studying cultures of explanted vagus nerves (day E11). These studies revealed that neural precursors were present in the vagi and gave rise in vitro to neurons that displayed acetylcholinesterase (AChE) activity and neuron-specific enolase (NSE) immunoreactivity. A subset of these neural precursors were capable of migrating and formed satellite ganglia at a distance from the explants. Coincident expression of NSE and TH immunoreactivities was observed, indicating that at least some of the neurons that developed in vitro were derived from TC cells. Vagal TC cells, therefore, are neurogenic. Catecholaminergic cells did not disappear from cultured explants of vagus nerves or gut provided that these tissues contained TC cells at the time of explantation. Instead, catecholaminergic neurons developed and persisted in vitro for as long as cultures were maintained. These neurons contained aromatic L-amino acid decarboxylase as well as TH, NSE and neurofilament immunoreactivities. In contrast, if the bowel was explanted after the in situ disappearance of TC cells, catecholaminergic cells did not arise in the cultures. These experiments indicate that the period of time during which a catecholaminergic phenotype is expressed by neural precursors in the fetal vagal pathway and gut is not fixed, but can be changed by altering the environment of the cells as occurs when the bowel is grown in vitro; moreover, contact with non-neuronal cells within the bowel is not by itself sufficient to inactivate catecholaminergic expression. The nature of the signal responsible for loss of the catecholaminergic phenotype in situ remains to be determined; however, the persistence of catecholaminergic expression in vitro should facilitate the investigation of this signal.
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PMID:Development and persistence of catecholaminergic neurons in cultured explants of fetal murine vagus nerves and bowel. 198 30

A descriptive enzyme histochemical study on the expression of acetylcholinesterase (AChE) in the developing rat spinal cord is presented. Between E11-E16, AChE was found to be associated with premitotic neurons of the ventral matrix layer, which indicated an involvement in the proliferation of the spinal cord motor neurons. From E12 on, AChE was abundantly present in the motor neurons of the ventral mantle layer, and in their fibres. This early expression suggested a function of AChE in the development of the motor neurons, rather than an active role in cholinergic transmission. The intermediolateral, the intermediomedial cell column and the region between these cell groups, were found to be positive for AChE. Cells of the adult intermediolateral cell column also expressed AChE. AChE, therefore, apparently plays a role in the development as well as in the functioning of the rat autonomic system. In the lateral funiculus, cells of the lateral spinal nucleus expressed AChE. After P8, AChE was expressed in the substantia gelatinosa. The enzyme may be associated with the fibre terminals of the primary afferents. AChE was found to be temporary expressed in the developing dorsal funiculus, which suggested a function of the enzyme in fibre growth and path-finding. At E12, AChE was located in the ventral aspect of the dorsal root ganglion. Later on, AChE positive cells were found throughout the ganglion.
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PMID:Acetylcholinesterase in the developing rat spinal cord: an enzyme histochemical study. 224 42

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

The development of the enteric nervous system was examined in fetal mice. Synthesis of [3H] acetylcholine ([3H]ACh) from [3H]choline and acetylcholinesterase histochemistry were used as phenotypic markers for cholinergic neurons, while the radioautographic detection of the specific uptake of [3H]serotonin (5-[3H]HT) and immunocytochemical staining with antiserum to 5-HT marked serotonergic neurons. The gut also was examined by light and electron microscopy. Development of the gut was studied in situ and in explants grown in organotypic tissue culture. Neurons were first detected morphologically in the foregut on embryonic day 12 (E12). Synthesis of [3H]ACh was detectable on days E10 to E12 but increased markedly between days E13 and E14. Uptake and radioautographic labeling by 5-[3H]HT was seen first in the foregut on day E12, in the colon on day E13, and in the terminal colon on day E14. Gut explanted from both distal and proximal bowel prior to the time when neurons could be detected (days E9 to E11) nevertheless formed neurons in culture. These cultures of early explants displayed markers for both cholinergic and serotonergic neurons. Enhances development of both cholinergic and serotonergic neurons was found in cultures explanted at day E11 over that found in cultures explanted on days E9 or E10. The evidence presented indicates (1) that enteric neurons develop from nonrecognizable precursors, (2) that the proximodistal gradient in neuronal phenotypic expression probably is not related to a proximodistal migration of precursor cells down the gut, (3) that the colonization of the bowel by neuronal precursors may be a prolonged process continuing from day E9 at least through day E11, (4) that the first pool of neuronal primordia to colonize the developing bowel can produce both cholinergic and serotonergic neurons. It is proposed that a sequential interaction of a long retained pool of dividing precursor cells with a fetal enteric microenvironment that changes as a function of time during ontogeny may be involved in producing the phenotypic diversity that characterized the enteric nervous system.
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PMID:Phenotypic expression in the developing murine enteric nervous system. 706 17

The development of acetylcholinesterase (AChE) activity and the distribution of this enzyme among its multiple forms was studied in both tissue extracts and dissociated cell cultures of chick paravertebral sympathetic ganglia. In agreement with previous findings, total AChE (expressed either per ganglion or per microgram protein) increased in vivo between the time of formation of the paravertebral chain (embryonic day 7; E7) to hatching (E20-E21). After this time, enzyme activity changed much more slowly. Sucrose gradient sedimentation analysis of AChE in ganglia of post-hatching chicks revealed multiple forms of AChE with S values of approximately 6.5, 11 and 19.5. Developmental studies showed that 6.5 S and 11 S forms are present as early as day E7. Much of the pre-hatching increase in total AChE is due to increased levels of the 6.5 S form of the enzyme. By hatching, this form comprised approximately 85-90% of the total AChE activity. In contrast, during the first week after hatching, the activity of the 11 S form increased several-fold while that of the 6.5 S remained approximately unchanged. The 19.5 S form, which is thought to be associated with the synaptic membrane, was not detected prior to day E17 and reached adult levels (2-3% of total AChE activity) by the first week after hatching. Development of AChE was also studied in dissociated cell cultures of embryonic ganglia. Essentially all the AChE activity in such cultures was found to be associated with the neurons. Total AChE activity of cultured E11 ganglia increased in a pattern which was both qualitatively and quantitatively similar to that which occurred in vivol. Furthermore, it was found that development of both the 6.5 and 11 S forms of AChE took place in vitro. In cultures of E8, E11, E15 and E19 ganglia, the distribution of activity between the two forms after various times in vitro was similar to that which was found for in vivo ganglia at an equivalent embryonic stage. Such changes were not affected by the elimination of nonneuronal cells from the cultures. Two aspects of in vitro development, however, differed from that which occurred in vivo. First, an increase in 11 S AChE did not occur at ages equivalent to the first week post-hatching. Second, the 19.5 S form did not develop (even after several weeks) in cultures of E8, E11 and E15 ganglia, nor was this form (which was removed during dissociation of the ganglia) regenerated in cultures of E19 ganglia. Such findings suggest that the pattern of development of AChE and its multiple forms in chick sympathetic neurons is in part intrinsically programmed into these cells at an early stage of development as well as in part regulated by extrinsic signals that these cells receive from their chemical and cellular environment.
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PMID:Development of the multiple molecular forms of acetylcholinesterase in chick paravertebral sympathetic ganglia: an in vivo and in vitro study. 735 92

Choline supplementation during fetal development [embryonic days (E) 11-17] permanently enhances memory performance in rats. To characterize the neurochemical mechanisms that may mediate this effect, we investigated the development of indices of the cholinergic system in the hippocampus: choline acetyltransferase (ChAT), acetylcholinesterase (AChE), synthesis of acetylcholine (ACh) from choline transported by high-affinity choline uptake (HACU), and potassium-evoked ACh release. During E11-E17, Sprague-Dawley pregnant rats consumed 0 [choline-deficient (ChD)], 1.3 [control (ChC)], and 4.6 [choline-supplemented (ChS)] mmol/(kg x day) of choline, respectively. On postnatal days 17 and 27, hippocampi of the ChD animals had the highest AChE and ChAT activities, and increased synthesis of ACh from choline transported by HACU, concomitant with reductions of tissue ACh content relative to the ChC and ChS rats and an inability to sustain depolarization-evoked ACh release relative to the ChS animals. In contrast, AChE and ChAT activities, and ACh synthesized from choline transported by HACU, were lowest in ChS rats whereas depolarization-evoked ACh release was the highest. This pattern of changes suggests that the hippocampus of the ChD animals is characterized by fast ACh recycling and efficient choline reutilization for ACh synthesis, presumably to maintain adequate ACh release despite the decrease of the ACh pool, whereas in the ChS animals ACh turnover and choline recycling is slower while the evoked release of ACh is high. Together, the data show a complex adaptive response of the hippocampal cholinergic system to prenatal choline availability and provide a novel example of developmental plasticity in the nervous system governed by the supply of a single nutrient.
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PMID:Prenatal availability of choline modifies development of the hippocampal cholinergic system. 950 79

Dorsal root ganglia (DRG) in the adult rat contain acetylcholinesterase (AChE) and butyrylcholinesterase (BChE), enzymes implicated in neural morphogenesis. We used quantitative histochemistry, reverse transcription-PCR (RT-PCR), and in situ hybridization histochemistry to study cholinesterase expression during embryogenesis. Longitudinal sections of rat embryos, embryonic day 9 (E9), E11-E17, and E19, were studied by video microscopy of the stained enzyme reaction products. Both enzymes were detectable in the early DRG (E11-E12), with BChE being most prominent. There was a spatiotemporal change in expression of each cholinesterase within the DRG. From E13 on, AChE expression predominated, especially in the neuronal cell bodies, while BChE was more highly expressed in the surrounding neuropil and the ganglionic roots. This distribution resembled the pattern in adult DRG. AChE mRNA levels, as determined by RT-PCR from DRG collected at days E12-E17, and E19, varied in parallel with the intensity of enzyme stain in the DRG. Overall, these results demonstrate temporally regulated ganglionic expression of cholinesterases, which may be important in the development of the sensory nervous system.
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PMID:Developmental expression of acetyl- and butyrylcholinesterase in the rat: enzyme and mRNA levels in embryonic dorsal root ganglia. 951 38

The vertebrate palatal muscles are derived from the cranial paraxial mesoderm and start myogenesis by the expression of myogenic regulatory factors (MRFs). Predetermined myogenic cells migrate from the cranial paraxial mesoderm into the branchial arches, followed by myogenic differentiation. The objective of this study was to elucidate whether the determination, migration, and differentiation of myogenic cells during the myogenesis of the palatal muscles, particularly the tensor veli palatini (TVP), are related to the extending mandibular nerve in mouse embryos. By immunohistochemical staining at embryonic day (E) 9.5, MyoD1 and myogenin have been expressed in the mandibular arch, into which the mandibular nerve had not yet extended. At E11.5, these myogenic cells encircled the extending mandibular nerve and were distributed from the distal and lateral to the trigeminal ganglion and into the mandibular arch to form the muscle plate, a girdle-like structure. By E12.5, these myogenic cells lost their girdle-like pattern, vacated the trunk area of the mandibular nerve, and were separated into several incompletely divided masses encircling the collateral branches of the mandibular nerve. The TVP started differentiation at E13.5 with the appearance of myofilaments and acetylcholinesterase (AchE), whereas the other palatal muscles began differentiation at E14.5. We defined the differentiation process of mouse palatal muscles into five stages based on the present findings. These results suggest that the determination and initial migration of the palatal myogenic cells into the mandibular arch occur before the mandibular nerve extends out of the trigeminal ganglion, whereas the myogenic cells migrating into the final sites of differentiation intimately relate to the extending nerve.
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PMID:Myogenic determination and differentiation of the mouse palatal muscle in relation to the developing mandibular nerve. 1043 29


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