Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.1.1.7 (acetylcholinesterase)
 28,390 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Involvement of phosphate-activated glutaminase in Huntington's disease and agonal state was investigated in caudate nucleus and frontal cortex from postmortem brains. In Huntington's disease the activities of phosphate-activated glutaminase, glutamic acid decarboxylase, succinic dehydrogenase, choline acetyltransferase, and acetylcholinesterase were significantly reduced in the caudate nucleus, but not in the frontal cortex. The activity of phosphate-activated glutaminase, and to a lesser extent of glutamic acid decarboxylase, was reduced in cases of terminal illness, as compared with cases of sudden death. Succinic dehydrogenase and choline acetyltransferase were reduced only in the few cases of prolonged and severe terminal illness. Enzyme activities of the caudate nucleus were more affected by agonal state than were those of frontal cortex. Results indicate that phosphate-activated glutaminase could be a useful marker of neuronal damage due to agonal state, and that phosphate-activated glutaminase and succinic dehydrogenase are reduced in Huntington's disease.
 ...
PMID:Phosphate-activated glutaminase in relation to Huntington's disease and agonal state. 622 89

Injections of the fluorescent dyes Fast Blue or Granular Blue into either the hippocampus (volume approximately 50 nl) or the entorhinal area (100-150 nl) resulted in labeling by retrograde axonal transport of cells in the diagonal band of Broca (dbB) and the medial septum (MS). A large number (approximately 30%) of these cells contained glutamic acid decarboxylase (GAD)-like immunoreactivity, as determined by combined retrograde fluorescent tracing and GAD-immunohistochemistry. Not all GAD positive cells in the dbB and MS were labeled by fluorochromes in a single experiment. The GAD-stained and fluorochrome-containing cells were present at all rostro-caudal levels of the septum and appeared not to belong to any single morphological class of cells. Double staining experiments showed that the GAD-positive cells did not contain acetylcholinesterase reaction product. These findings provide evidence that a significant portion of the septo-hippocampal projection may utilize gamma-aminobutyric acid as a neurotransmitter.
 ...
PMID:Septal neurons containing glutamic acid decarboxylase immunoreactivity project to the hippocampal region in the rat brain. 672 Dec 20

The addition of nerve growth factor (2.5S NGF) to serum-free aggregating cell cultures of fetal rat telencephalon greatly stimulated the developmental increase in choline acetyltransferase activity. Two other neuronal enzymes, acetylcholinesterase and glutamic acid decarboxylase, showed only slightly increased activities after NGF treatment whereas the total protein content of the cultures and the activity of 2',3'- cyclic nucleotide phosphodiesterase remained unchanged. The stimulation of choline acetyltransferase was dependent on the NGF media concentrations, showing a 50% maximum effect (120% increase) at approximately 3 ng/ml (10-10 M 2.5S NGF). NGF treatments during different culture periods showed that the cholinergic neurons remained responsive for at least 19 days. The continued treatment was the most effective; however, an initial treatment for only 5 days still caused a significant stimulation of choline acetyltransferase on day 19. The observed stimulation appeared to be specific to NGF. Univalent antibody fragments (Fab) against 2.5S NGF completely abolished the NGF-dependent increase in choline acetyltransferase activity, whereas Fab fragments of control IgG were ineffective. Furthermore, angiotensin II, added in high amounts to the cultures, showed no stimulatory effect. The present results suggest that certain populations of rat brain neurons are responsive to nerve growth factor.
 ...
PMID:Nerve growth factor (NGF) stimulation of cholinergic telencephalic neurons in aggregating cell cultures. 705 24

Rats were treated chronically with manganese chloride from conception onward for a period of over 2 years in order to study the effects of manganese and aging on the activities of glutamic acid decarboxylase (GAD), choline acetyltransferase (ChAT), and acetylcholinesterase (AChE) in hypothalamus, cerebellum, pons and medulla, striatum, midbrain, and cerebral cortex (which included the hippocampus). Manganese-treated 2-month-old and 24- to 28-month-old rats and age-matched controls were studied. In control rats during aging the activities of GAD decreased in hypothalamus (19%), pons and medulla (28%), and midbrain (22%) whereas the activities of AChE decreased in all regions (20-48%), particularly in the striatum (44-48%). Changes in ChAT activities in aging were observed only in one region-a decrease (23%) in the striatum. Life-long treatment with manganese appeared to abolish partially the decreases in aging in AChE activities in hypothalamus, cerebellum and striatum, and striatal ChAT activity. Manganese treatment also seemed to abolish the age-related decreases GAD activities, since GAD activities in various brain regions of manganese-treated senescent rats were not significantly different from those of control young rats. These results are discussed in relation to other metabolic changes associated with aging and manganese toxicity.
 ...
PMID:Brain regional distribution of glutamic acid decarboxylase, choline acetyltransferase, and acetylcholinesterase in the rat: effects of chronic manganese chloride administration after two years. 726 41

Triiodothyronine (30 nM) added to serum-free cultures of mechanically dissociated re-aggregating fetal (15-16 days gestation) rat brain cells greatly increased the enzymatic activity of choline acetyltransferase and acetylcholinesterase throughout the entire culture period (33 days), and markedly accelerated the developmental rise of glutamic acid decarboxylase specific activity. The enhancement of choline acetyltransferase and acetylcholinesterase specific activities in the presence of triiodothyronine was even more pronouned in cultures of telencephalic cells. If triiodothyronine treatment was restricted to the first 17 culture days, the level of choline acetyltransferase specific activity at day 33 was 84% of that in chronically treated cultures and 270% of that in cultures receiving triiodothyronine between days 17 and 33, indicating that relatively undifferentiated cells were more responsive to the hormone. Triiodothyronine had no apparent effect on the incorporation of [3H]thymidine at day 5 or on the total DNA content of cultures, suggesting that cellular differentiation, rather than proliferation was affected by the hormone. Our findings in vitro are in good agreement with many observations in vivo, suggesting that rotation-mediated aggregating cell cultures of fetal rat brain provide a useful model to study thyroid hormone action in the developing brain.
 ...
PMID:Triodothyronine enhancement of neuronal differentiation in aggregating fetal rat brain cells cultured in a chemically defined medium. 741 92

Neurochemical analysis of neuronal function was undertaken by measuring the activities of cholinacetyltransferase (CAT), acetylcholinesterase (AChE), and glutamic acid decarboxylase (GAD), in the telencephalon, brain stem and cerebellum of the mouse. Cholinergic activity was first expressed in the 10-day embryonic brain stem, which showed a relatively high CAT activity at birth. Postnatal brain stem development was characterized by a rapid and parallel increase in CAT and AChE. Although AChE peaked at 1 month, CAT activity was no achieved until 1 year. Acetylcholine synthesis was initiated in the 12-day embryonic telencephalon and a steady age-related increase in CAT was maintained until birth. A lag in both CAT and AChE activities was recorded during the first week of postnatal telencephalon development. Cerebellar CAT was low at birth, and increased irregularly to reach a maximum by 1 month. In contrast, postnatal cerebellar AChE activity increased steadily over the same time period. The GABA-ergic neuronal system matured rapidly in each brain region, and was unaffected by aging. Although the brain stem precociously expressed cholinergic activity, it wa the region most susceptible to deterioration during aging. Telencephalon CAT activity was unaffected by aging and in the cerebellum, a significantly reduced level of CAT was only found in truly senescent animals. The decreased cholinergic function during senescence was not due to either increased proteolysis or to alteration in the molecular form of the cholinergic enzymes.
 ...
PMID:Neurotransmitter enzymes in telencephalon, brain stem and cerebellum during the entire life span of the mouse. 742 Dec 99

Mouse embryonic stem cells were induced to differentiate in culture with retinoic acid. Putative precursors of neurons and glial cells (nestin-positive cells) were clearly identified as early as three days after the onset of differentiation. At day 6, neuron-like cells could be clearly identified, either as isolated cells or as cellular networks. Some of these cells were positive for astrocyte- or oligodendrocyte-specific antigens (GFAP or O4 antigens, respectively). Other cells were positive for neuron-specific antigens (cytoskeleton proteins MAP2, MAP5 and NF200, as well as synaptophysin). Some neuronal-like cells were also positive for acetylcholinesterase activity or glutamic acid decarboxylase expression, indicating that ES cells could differentiate into GABAergic and possibly cholinergic neurons. Electrophysiological analyses performed in voltage clamp conditions showed that cell membranes contained voltage-dependent channels. Overshooting action potentials could be triggered by current injection. Taken together, these data provide evidence that embryonic stem cells can differentiate first into neuron-glia progenitors, and later into glial cells and functional neurons, in vitro. This technique provides an unique system to study early steps of neuronal differentiation in vitro.
 ...
PMID:In vitro differentiation of embryonic stem cells into glial cells and functional neurons. 759 79

Congenital ornithine transcarbamylase (OTC) deficiency in humans is associated with seizures and mental retardation. As part of a series of studies to delineate the neurochemical features of OTC deficiency, activities of choline acetyltransferase (ChAT) and acetylcholinesterase (AChE), respectively, were measured in brain regions of the congenitally hyperammonemic sparse-fur (spf) mouse, a mutant with an X-linked inherited defect of OTC. ChAT activities were reduced by 63% (P < 0.01) in cerebral cortex of spf mice compared with CD-1/Y controls. Activities of the GABA nerve terminal marker enzyme, glutamic acid decarboxylase, on the other hand, were within normal limits. Using an immunohistochemical technique with a monoclonal antibody to ChAT, a significant loss of ChAT-positive neurons was observed throughout the cerebral cortex, septal area and diagonal band of spf mice. These results suggest that a loss of forebrain cholinergic neurons is a feature of congenital OTC deficiency in these mutants. Possible pathogenetic mechanisms responsible for the cholinergic neuronal loss in congenital OTC deficiency include neurotoxic effects of ammonia and accumulation of quinolinic acid.
 ...
PMID:Evidence for cholinergic neuronal loss in brain in congenital ornithine transcarbamylase deficiency. 781 42

This study describes the cellular distribution of muscarinic acetylcholine receptors (mAChRs) in the medial septum (MS), employing the monoclonal antibody M35 raised against purified mAChR-protein. mAChR-positive neurons are found throughout the MS, but are predominantly located in the midline area and in the lateral compartments. The labeled cell bodies are variable in shape and size (largest diameter ranging from 10-30 microns), while both soma and the associated dendritic processes are densely stained for mAChRs. Astrocytes immunoreactive for mAChRs were frequently found associated with the large blood vessels in the midline area. To study the neurotransmitter nature of the mAChR-positive cells, immunofluorescence double-labeling experiments were performed for mAChRs and GABAergic and cholinergic markers. GABAergic cells were identified immunocytochemically using antisera against glutamic acid decarboxylase (GAD), parvalbumin (PARV) or calbindin protein (CaBP). The cholinergic transmitter nature of the mAChR-positive cells was studied using adjacent 8 microns thick serial sections stained immunocytochemically for choline acetyltransferase (ChAT), or histochemically for acetylcholinesterase (AChE). These experiments showed that approximately half (52.3%) of all mAChR-positive cells contain GAD, whereas the other half is cholinergic. Conversely, nearly all GABAergic (98.6%) and cholinergic (96.9%) cells are endowed with mAChRs. GAD-positive terminals were found surrounding mAChR-positive perikarya which were either GAD-positive or GAD-negative, indicating GABAergic innervation on both GABAergic and cholinergic MS neurons. In general, the staining intensity for mAChRs appeared to be considerably higher in GABAergic than in cholinergic neurons, suggesting a stronger cholinergic impact upon the GABAergic neurons. The current anatomical findings contribute to the concept that the MS neurons form a firmly interconnected cell group, in which cholinergic neurotransmission mediated through mAChRs seems to play a significant role.
 ...
PMID:Cholinergic and GABAergic neurons in the rat medial septum express muscarinic acetylcholine receptors. 795 39

Numerous studies suggest that growth and trophic factors play roles in the development and mature function of brain neurons. Recently, growth factors whose actions were previously characterized on non-neuronal cells have been localized to the brain. We sought to determine whether these factors influence septal cholinergic function. Initially, we defined the effects of basic fibroblast growth factor (bFGF) and epidermal growth factor (EGF) on septal cholinergic cells in dissociated neuronal culture. Both factors elevated activity of the acetylcholine synthetic enzyme, choline acetyltransferase (CAT). To determine whether the factors acted directly on neurons or whether glia mediated the effects, a mitotic inhibitor, 5-fluorodeoxyuridine (FDUR), was added to the cultures to eliminate dividing glia. The action of EGF was completely blocked by the addition of FDUR. However, bFGF elevated CAT activity even in the presence of FDUR. Consequently, bFGF may regulate septal cholinergic function directly, whereas EGF may affect cholinergic cells indirectly through glia. To determine whether increases in CAT activity reflect increased enzyme activity per neuron or an increase in the number of cholinergic cells, bFGF-treated cultures were stained for acetylcholinesterase (AChE) to determine numbers of cholinergic cells. No differences in AChE-positive cells were noted, suggesting that bFGF increased CAT activity per cholinergic neuron. To determine whether bFGF regulates other populations in the septum, we examined GABAergic neurons by monitoring the activity of glutamic acid decarboxylase (GAD), a GABA synthetic enzyme. Basic FGF significantly increased GAD activity; however, the effect was completely abolished by addition of FDUR. Thus, bFGF may act directly on cholinergic neurons and indirectly on GABA cells.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Septal neuron cholinergic and GABAergic functions: differential regulation by basic fibroblast growth factor and epidermal growth factor. 802 75


<< Previous 1 2 3 4 5 6 Next >>