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

The activity of choline acetyltransferase (ChAT), acetylcholinesterase (AChE), and muscarinic receptors was studied in control rats and in rats growth-retarded in utero because of reduction of the blood supply 5 days before birth. The different markers of the cholinergic system were estimated at P (postnatal day) 6, 9, 12, 15, 22 and 60 in cerebellum, hypothalamus, septum, striatum and CA1, CA3 and fascia dentata of the hippocampus. In control rats, there was a transient increase in ChAT activity in the septum during the second week of postnatal development. In the intrauterine growth retarded rats there was a marked delay in this developmental rise in CA1, CA3 at P6 and P9 and in the fascia dentata at P14 respectively. This delayed rise enzyme activity was associated with a significant reduction of muscarinic binding sites [( 3H]QNB) in the hippocampus. AChE staining showed a similar development in both groups. Therefore, the undernutrition produced by a reduction of the blood supply 5 days before birth is associated with a delayed maturation of cholinergic functions.
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PMID:Development of the cholinergic system in control and intra-uterine growth retarded rat brain. 273 67

Nerve growth factor (NGF), a well-characterized target-derived growth factor, has been postulated to promote neuronal differentiation and survival of the basal forebrain cholinergic neurons. In the present paper, we demonstrate that a developmental change in NGF action occurs in postnatal rat basal forebrain cholinergic neurons in culture. Firstly, NGF acts as maturation factor by increasing choline acetyltransferase (ChAT) activity and acts later as a survival factor. In dissociated cell cultures of septal neurons from early postnatal (P1-4) rats, ChAT activities were increased by the addition of NGF. That is, ChAT activities in P1 septal cells cultured for 7 days was increased 4-fold in the presence of NGF at a concentration of 100 ng/ml. However, the number of the acetylcholinesterase (AChE)-positive neurons was not significantly different between these groups. In contrast, septal neurons from P8 to P14 rats showed different responses to NGF. Although the P14 septal neurons in culture for 7 days without NGF lost about half of the ChAT activity during a 7-day cultivation, cells cultured with NGF retained the activity at the initial level. The number of AChE-positive neurons counted in cultures with NGF was much greater than the number without NGF. These results suggest that, during the early postnatal days, the action of NGF on the septal cholinergic neurons in culture changes from induction of ChAT activity to the promotion of cholinergic neuronal cell survival. During this developmental period in vivo, septal neurons are terminating their projections to the hippocampal formation. Similar NGF-regulated changes in cholinergic neurons were observed in cultured postnatal neurons from vertical limb of diagonal band. An analogy has been pointed out between the neuronal death of the basal forebrain cholinergic neurons and a similar neuronal death in senile dementia, especially Alzheimer's type. The work reported here might present a possibility that NGF could play a role in preventing the loss of the basal forebrain cholinergic neurons in this disease.
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PMID:Developmental change in the nerve growth factor action from induction of choline acetyltransferase to promotion of cell survival in cultured basal forebrain cholinergic neurons from postnatal rats. 335 32

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

The function of acetylcholinesterase (AChE) is to terminate the action of acetylcholine at the cholinergic synapse. Recent evidence suggests additional roles for acetylcholinesterase as a peptidase and/or a protease which is expressed by growing neurites as part of their invasion of developing neural structures. We report the localization of acetylcholinesterase in developing ferret retina. AChE histochemical staining is seen in the developing inner plexiform layer (IPL) of ferret retina at birth (post-natal day zero, PO), the earliest developmental stage examined. Transient expression is seen at the border between the ganglion cell layer and the nerve fiber layer at P14 and P21. A small amount of transient expression is seen in the outer plexiform layer (OPL) at this age as well. By P28, the transient expression in the OPL is at its peak, and is found at photoreceptor terminals and associated with apparent horizontal cell axons. Labeling is also seen intracellularly in the inner nuclear layer (INL), at the OPL/INL border, suggesting that horizontal cells are the source of the transient AChE expression in the OPL. Overt synaptic profiles also appear in the inner plexiform layer (IPL) at P21 and P28. About 2 days layer, the eyes open and the photoreceptor outer segments are fully developed. By 2 weeks later, at P42, the AChE staining pattern in the retina has taken on its adult appearance: no reaction product in the outer retina; intracellular reaction product in the Golgi apparatus of a subset of amacrine and displaced amacrine cells which manufacture AChE; and extracellular reaction product at both synaptic and non-synaptic sites in the IPL. These data are consistent with a role for AChE as a peptidase early in development, and as an enzyme essential in the termination of synaptic action at mature synapses.
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PMID:Acetylcholinesterase in the developing ferret retina. 778 40

The effects of nerve growth factor (NGF) and a blocking anti-NGF antibody were studied in cultures plated from postnatal day 1-28 (P1-P28) rat septum and maintained 3 weeks in vitro. 7S NGF (100 ng/ml = 0.75 nM) increased choline acetyltransferase (ChAT) activity in P7-P21 cultures. The largest increase was measured in P7-P14 cultures, where NGF addition produced ChAT activities 5-12 times higher than those measured in cultures grown in anti-NGF antibody. NGF also increased the number of acetylcholinesterase (AChE)-positive neurons in P7-P14 cultures. To determine whether this increase was due to enhanced survival of cholinergic neurons or simply to enhanced AChE expression, we examined cultures to which NGF was added only after an initial 1-2-week exposure to anti-NGF antibody. This delayed addition of NGF also increased ChAT activity and the number of AChE-positive neurons, indicating that cholinergic neurons survived the initial exposure to anti-NGF antibody. Thus even during a period when ChAT activity was most sensitive to NGF, postnatal septal cholinergic neurons did not require NGF for survival in vitro.
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PMID:Changes in the response of cultured septal cholinergic neurons to nerve growth factor exposure and deprivation during the first postnatal month. 795 20