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)

A quantitative acetylcholinesterase enzyme-histochemical study was performed with microdensitometric methods in the hippocampus of the rat in order to correlate this enzymatic activity with the different zones of the hippocampal pyramidal layer. Higher values of acetylcholinesterase activity were found in the CA3 pyramidal zone. CA1 and CA4 showed the same activity, while the stratum oriens at CA3 showed the highest values among the hippocampal layers studied. The results were correlated with differences in septal afferences.
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PMID:Microdensitometry of acetylcholinesterase in subfields of the hippocampal pyramidal layer and fascia dentata. 43 69

In rats learning to use nonpreferred paw is accompanied by an increase of acetylcholinesterase (AChE) of specific areas of rat cerebral cortex and pyramidal neurones of CA3 and CA4 of the hippocampus. Following achievement of new behavioural reactions high AChE activity is preserved longer in the neacortex, the enzyme activity in the pyramidal neurones of the hippocampal cortex coming to normal. Following preliminary intracranial administration of puromycin the increase of AChE activity during learning is no more observed. This indicates the activation of the genetic apparatus during learning and training as a result of which synthesis of membrane proteins including AChE is enhanced. A close correlation between learning and the inductive synthesis of AChE is observed. Lateralization of the chemical traces of learning in specific areas of rat cerebral cortex are observed as increased activity of AChE. Changes in AChE activity in various hemispheres of rat brain during learning are thought to be due to assymetric changes in the excitatory level of cortical sites during the formation of new behavioural reactions. The specific localization of biochemical changes in the brain is certainly more favorable from an energetic aspect and may by regarded as an evolutionary compensatory process. The interrelationship of the activation of the synthetic apparatus of the cell with the reception of external informations is one of the expressions of adaptation during codations of functions of the organism more advantageous from an evolutionary point of view.
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PMID:[Inductive synthesis of acetylcholinesterase in the brain during learning and training of rats]. 123 73

The biochemical and morphological effects of postnatal acetylcholinesterase (AChE) inhibition were examined in rat pups dosed with parathion, at time points critical to hippocampal neurogenesis and synaptogenesis (i.e., day 5-20). In treated pups, sacrificed on day 21, hippocampal histopathology, as assessed by light and electron microscopy, consisted of cellular disruption and necrosis in the dentate gyrus (DG), and CA4 regions. Synaptic disruption in the DG molecular layer was suggested by histochemical preparation using both the Timm's and AChE stains. In parathion-treated pups, sampled at day 12, hippocampal AChE was depressed 73% and [3H] quinuclidinyl benzilate (QNB) binding was depressed by 36%. The above results indicate that morphological and biochemical consequences are associated with persistent AChE depression in neonatal rats.
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PMID:The neurotoxicity of parathion-induced acetylcholinesterase inhibition in neonatal rats. 208 86

The biochemical and morphological effects of postnatal acetylcholinesterase (AChE) inhibition were examined in rat pups dosed with paration, at time points critical to hippocampal neurogenesis and synaptogenesis (i.e., day 5-20). In treated pups, sacrificed on day 21, hippocampal histopathology, as assessed by light and electron microscopy, consisted of cellular disruption and necrosis in the dentate gyrus (DG), and CA4 regions. Synaptic disruption in the DG molecular layer was suggested by histochemical preparation using both the Timm's and AChE stains. In parathion-treated pups, sampled at day 12, hippocampal AChE was depressed 73% and [3H] quinuclidiny benzilate (QNB) binding was depressed by 36%. The above results indicate that morphological and biochemical consequences are associated with persistent AChE depression in neonatal rats.
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PMID:The neurotoxicity of parathion-induced acetylcholinesterase inhibition in neonatal rats. 228 52

Unilateral fimbria-fornix lesions were made by aspiration in female Sprague-Dawley rats. In a group of these rats, fetal septal tissue was transplanted into the lesion cavity. Lesion of the fimbria-fornix resulted in a reduction of cholinergic input to the hippocampal formation as indicated by the loss of acetylcholinesterase (AChE)-positive staining in all ipsilateral hippocampal laminae and a loss of [3H]hemicholinium-3 binding to cholinergic terminals in the strata oriens (82% reduction) and radiatum (77% reduction) of areas CA2 and CA3 and in the molecular layer of the dentate gyrus (83% reduction). In contrast, the density of muscarinic receptor binding ([3H]QNB) increased in the strata oriens (80% increase) and radiatum (70% increase) in areas CA2-CA4. This was shown to be due to an actual increase in receptor number (Bmax) and not to a change in affinity (KD). Analysis of muscarinic receptor subtypes indicated that the increase in receptor binding in the stratum radiatum was of the M-1 subtype ([3H]-pirenzepine) and in the stratum oriens was of the M-2 subtype ([3H]QNB + 100 nM pirenzepine). In the host hippocampus after fetal septal graft, the staining for AChE, the binding of [3H]hemicholinium-3, and the binding of muscarinic receptors (both the M-1 and M-2 receptor subtypes) were all comparable to nonlesioned control values. These data indicate that the fetal septal grafts have reinnervated the host hippocampus and have made synaptic contact with host cells in a manner capable of regulating postsynaptic muscarinic receptors.
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PMID:Normalization of subtype-specific muscarinic receptor binding in the denervated hippocampus by septodiagonal band grafts. 280 54

A series of experiments was conducted to characterize the long term behavioural consequences of acute intoxication with trimethyltin (TMT) (5,6,7, mg/kg p.o.). The acute toxicity syndrome, including weight loss, convulsions, irritability and hyper-reactivity was confirmed in treated rats. These symptoms subsided to reveal marked increases in locomotor activity in a novel environment but no lasting effects on consummatory behaviour or sensorimotor integration. Neither two-way active avoidance nor passive avoidance learning were impaired by doses of up to 7 mg/kg p.o. although intertrial activity was elevated in the shuttle box and extinction responding was increased. Place navigation in a water maze was impaired, particularly at the highest dose of TMT (7 mg/kg p.o.) and when a brief training phase (8 trials) was used. Finally, TMT lesioned rats were compared with controls on spatial and non-spatial discrimination tasks. Following 7 mg/kg p.o. TMT rats were highly impaired on the spatial discrimination but not the non-spatial discrimination despite the greater difficulty of the latter task. Histological studies confirmed the pathological effects of TMT in limbic structures, particularly the pyramidal cells of CA1 and CA4, and also revealed increased acetylcholinesterase activity within the molecular layer of the dentate gyrus. The selective, long term behavioural impairments caused by TMT are discussed in the light of their qualitative similarity to the effects of hippocampectomy or hippocampal denervation. TMT lesioned rats may provide a suitable functional model for the partial hippocampal and temporal lobe pathology characteristic of Alzheimer's disease.
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PMID:Selective behavioural impairment after acute intoxication with trimethyltin (TMT) in rats. 339 3

Neuropathological and biochemical effects of neonatal exposure to the alkyl metal triethyltin were examined in juvenile male Long Evans rats. Rats were injected intraperitoneally on postnatal day 5 with 6 mg/kg of triethyltin bromide and sampled on day 20. The brains of tin-treated animals weighed significantly less than either saline or starved controls and exhibited a marked caviation of the ventrolateral surfaces. Histologically, neuronal necrosis was noted in the entorhinal and transitional cortex, an observation confirmed by immunocytochemical staining of astrocytes. Hippocampal involvement was further evidenced by a protrusion of the molecular layer of the dentate gyrus, and an abnormal histochemical staining pattern of acetylcholinesterase in this layer. Sections stained by the Timm's method for the deposition of heavy metals showed a marked reduction in the staining of the hippocampal CA4,3,2 sectors and an absence of stained laminae in the outer molecular layer of the dentate gyrus. Receptor binding assays indicated a selective depression of the benzodiazepine receptor in the hippocampus of tin-treated pups compared to starved controls. Taken in concert, these data indicate that neonatal exposure to triethyltin produces severe neuronal damage in the posterior cortex and a derangement of hippocampal afferent circuitry.
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PMID:Triethyltin-induced neuronal damage in neonatally exposed rats. 371 27

The cholinergic innervation of the hippocampal formation is thought to play an important role in memory processes, but its organization in humans has not been described in detail. We studied the cholinergic innervation of the human hippocampal formation by means of immunohistochemistry with polyclonal antisera directed against acetylcholinesterase (AChE), choline acetyltransferase (ChAT), and the low-affinity (p75) nerve growth factor receptor (NGFR). The density of ChAT-like immunoreactive (ChAT-li) fibers differed substantially among the various regions, in general paralleling the pattern of AChE-li staining. One notable exception was the presence of AChE-li cell bodies. In contrast, ChAT immunoreactivity was associated only with fibers and terminals. NGFR-li staining corresponded closely to the ChAT-li fiber pattern. ChAT-li fibers in the CA fields diffusely filled the stratum pyramidale and extended into the stratum oriens and radiatum as well. The highest density was consistently observed in CA4 and CA3 subfields. Staining decreased from CA4 to CA1 and was substantially less dense in the subicular complex. In the entorhinal cortex, the ChAT- and NGFR-li fiber innervation displayed a laminar pattern, most intense over the nests of cells in layer II. There was a trend towards an age-related reduction in the density of ChAT- and AChE-li fibers and terminals. Nonetheless, we also found a surprisingly conserved NGFR-li innervation and the presence of occasional NGFR-li pyramidal cells, providing evidence of a plastic response in the brains of the elderly patients.
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PMID:Cholinergic innervation in the human hippocampal formation including the entorhinal cortex. 792 5

The vulnerability of the human hippocampal complex to disease, trauma, and aging indicates the necessity to target this area therapeutically. The distribution and density of transmitter receptors provide a rational basis for this approach, and in this study the topography of 11 different pharmacological sites is compared with the cholinergic innervation, which is particularly vulnerable in dementia. The regional distribution of cholinergic innervation to the normal adult human hippocampus and adjacent cortex, marked by acetylcholinesterase (AChE) fiber and terminal reactivity, is notable for its concentration in CA2/3 of Ammon's horn and the dentate fascia. Neither nicotinic (high-affinity nicotine binding) nor muscarinic ("M1" or "M2") cholinergic receptor binding paralleled this distribution. In Ammon's horn, 5-HT2 and kainate receptor binding more closely resembled the pattern of AChE, being concentrated in CA2-4 compared with CA1. By contrast, muscarinic M1 and M2, 5-HT1A, benzodiazepine (including zolpidem-insensitive binding), NMDA (MK801), and AMPA/QUIS receptors were higher in CA1 and/or subiculum. Kainate binding, like AChE, was high in CA4. 5-HT2 and nicotinic binding partially mimicked the pattern of AChE around the granule layer. In the subicular complex and parahippocampal gyrus, where cholinergic activity is relatively lower, muscarinic, 5-HT1A, and benzodiazepine binding were relatively high and the nicotinic receptor was remarkable for its highest density compared to other areas examined. In stratum lacunosum-moleculare of CA1, which was relatively low in AChE activity, there was a dense band of nicotinic, M2, and benzodiazepine receptor binding.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Autoradiographic comparison of cholinergic and other transmitter receptors in the normal human hippocampus. 839 72

Ontogenic development of muscarinic receptors was examined in the hippocampus of rabbits (from P2 to P60) using radioautographic method. Muscarinic sites were labelled with (3H)-quinuclinidyl-benzilate and pharmacologically defined M1 and M2 receptor subtypes with (3H)-pirenzepine and (3H)-oxotremorine, respectively. The distribution of binding sites was compared to acetylcholinesterase (AChE) staining in adjacent hippocampal sections. The two cholinergic components are progressively set up in the hippocampus during the first three postnatal weeks. The AChE staining was very low in all hippocampal fields in P2 rabbits. At P8 and after, the AChE staining was more pronounced in CA3 and CA4 than in CA1 and CA2. On the contrary, the M1 muscarinic binding sites were more abundant in CA1 and CA2 hippocampal fields than in CA3 and CA4 at all ages studied. M2 muscarinic binding sites were only distinguishable at P45 and have a relatively homogeneous distribution. This study shows a differential developmental evolution in the distribution of AChE and muscarinic M1 receptors, and no obvious correspondence between these two cholinergic markers was observed.
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PMID:Ontogenic distribution of muscarinic receptors and acetylcholinesterase in the rabbit hippocampus. 851 62


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