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)

Animal experiments have already shown that neurotransmitters and neuropeptides are not only important for normal functioning of the adult central nervous system (CNS) but are also crucial to its development. However, information on the spatio-temporal distribution of these endogenous substances in the developing human CNS is still scarce. With the use of immunocytochemical staining and a constant supply of properly fixed human abortuses from southern China, an early appearance of acetylcholinesterase, enkephalin, and substance P immunoreactivities was detected first in the spinal cord (weeks 5 to 7 of gestation), then in the brainstem nuclei (weeks 11 to 12). Their overlapping localizations in many regions of the CNS suggest possible interactions among neurons containing these substances, which are in turn important for the proper establishment of the neuronal circuitry. Immunoreactivity for neuropeptide Y appeared initially in the lateral region of upper segments of the spinal cord at week 12 of gestation, then spread latero-medially and cranio-caudally to the sacral region. In the hippocampus, neuropeptide Y neurons appeared from week 15 onwards. Serotoninergic neurons were found in the dorsal raphe nucleus at week 10 and then decreased in number as the fetus grew older. Somatostatin releasing inhibitory factor, vasopressin, and oxytocin were detected in the hypothalamus from weeks 12 to 14 onwards, and monoamine oxidase, succinic dehydrogenase, parvalbumin, calbindin D28K, and vasoactive intestinal peptide were found in the visual cortex at midgestation. The early appearance and the abundance of the neurotransmitters and neuropeptides in the developing CNS indicate that they may play a key role in neuronal differentiation.
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PMID:Early appearance of acetylcholinergic, serotoninergic, and peptidergic neurons and fibers in the developing human central nervous system. 1040 66

The neurochemical organization of the striosomal compartment in the human striatum was analyzed by histochemical and immunohistochemical techniques applied to postmortem tissue from normal individuals. The striosomes were delineated by using the following markers: acetylcholinesterase (AChE), enkephalin (ENK), substance P (SP), calbindin-D28k (CB), parvalbumin (PV), calretinin (CR), limbic system-associated membrane protein (LAMP), choline acetyltransferase (ChAT), tyrosine hydroxylase (TH), and NADPH-diaphorase. Comparisons were made between striosomal boundaries, as outlined by each marker applied on adjacent sections, and particular attention was paid to possible variations in the chemical features of striosomes along the rostrocaudal extent of the striatum. The main findings of this study are as follows: 1) the striosomal compartment is composed of two chemically distinct domains: a core and a peripheral region; 2) the core is largely devoid of CB and displays a less intense staining for ENK and LAMP than the peripheral region; 3) although striosomes are largely devoid of AChE, the activity of this enzyme is slightly higher in the core than in the peripheral region; 4) the core and peripheral regions are weakly stained for PV and intensely stained for SP; 5) ChAT-, CR- and NADPH-diaphorase-positive neurons are preferentially distributed in the peripheral region; 6) at rostral striatal levels, striosomes are largely devoid of TH, whereas the inverse is true caudally; and 7) at caudal striatal levels, the peripheral region of striosomes is intensely stained for CB and ChAT. These results demonstrate that the striosomes in human display a strikingly complex and heterogeneous chemical architecture.
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PMID:Chemical heterogeneity of the striosomal compartment in the human striatum. 1049 46

To investigate the organization of the dorsal pulvinar complex, patterns of neurochemical staining were correlated with cortico-pulvinar connections in macaques (Macaca mulatta). Three major neurochemical subdivisions of the dorsal pulvinar were identified by acetylcholinesterase (AChE) histochemistry, as well as immunostaining for calbindin-D(28K) and parvalbumin. The dorsal lateral pulvinar nucleus (PLd) was defined on histochemical criteria as a distinct AChE- and parvalbumin-dense, calbindin-poor wedge that was found to continue caudally along the dorsolateral edge of the pulvinar to within 1 mm of its caudal pole. The ventromedial border of neurochemical PLd with the rest of the dorsal pulvinar, termed the medial pulvinar (PM), was sharply defined. Overall, PM was lighter than PLd for AChE and parvalbumin and displayed lateral (PMl) and medial (PMm) histochemical divisions. PMm contained a central "oval" (PMm-c) that stained darker for AChE and parvalbumin than the surrounding region. The neurochemically defined PLd was labeled by tracer injections in the inferior parietal lobule (IPL) and dorsolateral prefrontal cortex but not the superior temporal gyrus (STG). Label within PMl was found after prefrontal and IPL and, to a lesser extent, after STG injections. The PMm was labeled after injections of the IPL and STG, but only sparsely following prefrontal injections. The histochemically distinct subregion or module of PMm, PMm-c, was labeled only by STG injections. Overlapping labeling was found in dorsal pulvinar divisions PMl and PLd following paired IPL/prefrontal, but not IPL/STG or these particular STG/prefrontal, injections. Thus, PLd may be a visuospatially related region whereas PM appears to contain several types of territories, some related to visual or auditory inputs, and others that receive directly converging input from posterior parietal and prefrontal cortex and may participate in a distributed cortical network concerned with visuospatial functions.
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PMID:Neurochemical and connectional organization of the dorsal pulvinar complex in monkeys. 1071 40

Many endogenous neurochemicals that are known to have important functions in the mature central nervous system have also been found in the developing human cerebellum. Cholinergic neurons, as revealed by immunoreactivities towards choline acetyltransferase or acetylcholinesterase, appear early at 23 weeks of gestation in the cerebellar cortex and deep nuclei. Immunoreactivities gradually increase until the first postnatal month. Enkephalin is localized in the developing cerebellum, initially in the fibers of the cortex and deep nuclei at 16-20 weeks and then also in the Purkinje cells, granule cells, basket cells and Golgi cells at 23 weeks onward. Another neuropeptide, substance P, is localized mainly in the fibers of the dentate nucleus from 9 to 24 weeks but substance P immunoreactivity declines thereafter. GABA, an inhibitory neurotransmitter of the central nervous system, starts to appear at 16 weeks in the Purkinje cells, stellate cells, basket cells, mossy fibers and neurons of deep nuclei. GABA expression is gradually upregulated toward term forming networks of GABA-positive fibers and neurons. Catecholaminergic fibers and neurons are also detected in the cortex and deep nuclei at as early as 16 weeks. Calcium binding proteins, calbindin D28K and parvalbumin, make their first appearance in the cortex and deep nuclei at 14 weeks and then their expression decreases toward term, while calretinin appears later at 21 weeks but its expression increases with fetal age. The above findings suggest that many neurotransmitters, neuropeptides and calcium binding proteins (1) appear early during development of the cerebellum; (2) have specific temporal and spatial expression patterns; (3) may have functions other than those found in the mature neural systems; and (4) may be able to interact with each other during early development.
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PMID:Neurotransmitters, neuropeptides and calcium binding proteins in developing human cerebellum: a review. 1112 73

In the Madagascan hedgehog tenrec, Echinops telfairi, the entire paleocortical region (PCx) subjacent to the rhinal indentation is composed of three layers and occupies up to two thirds of the lateral hemisphere. A clear differentiation of PCx into its presumed constituents, the piriform cortex and the entorhinal cortex, as seen in other mammals, has not been obtained so far. To gain insight into location and intrinsic organization of these areas in a basal placental mammal we investigated the tenrec's PCx using cyto-, myelo- and chemoarchitectural criteria (zinc, acetylcholinesterase, NADPh-diaphorase, Wisteria floribunda agglutinin, parvalbumin, calbindin, calretinin) and analysed its connections with the olfactory bulb. The layers 2 and 3 of the tenrec's PCx differed from the corresponding layers in the rat. The layer 2 showed a complex distribution of corticobulbar cells but could not be subdivided, in contrast to layer 3. Additional cell groups in the depth of PCx were tentatively compared with subdivisions of the endopiriform region. The architectural and connectional features varied clearly along the rostrocaudal and dorso-ventral extents of PCx and gave hints for the presence of different paleocortical subdivisions. With the possible exception of an area located at the most caudal tip of the dorsomedial hemisphere, however, no conclusive evidence was obtained for the presence of a multilayered, entorhinal region. The bulbar projections to the PCx were very extensive and almost exclusively ipsilateral. The laterality of the projection is similar to that in higher mammals, but differs from that in the erinaceous hedgehog.
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PMID:The subrhinal paleocortex in the hedgehog tenrec: a multiarchitectonic characterization and an analysis of its connections with the olfactory bulb. 1113 Oct 16

Based on cytoarchitectonic criteria, the primate pulvinar nucleus has been subdivided into medial (PM), lateral (PL), and inferior (PI) regions. However, these subdivisions show no correlation with those established by electrophysiological, immunocytochemical, or neuroanatomical tracer studies. In this work, we studied the connections of the pulvinar nucleus of Cebus monkey with visual areas V1, V2, V4, MT, and PO by means of retrograde fluorescent tracers injected into these areas. Based on the projection zones to cortical visual areas, the visual portion of the pulvinar of Cebus monkey was subdivided into three subregions: P1, P2, and P3, similar to those described in the macaque (Ungerleider et al., 1984). In Cebus, P1 includes the centrolateral portion of traditionally defined PI and adjacent portion of PL. P2 is located in the dorsal portion of PL and P3 includes the medial portion of PI and extends dorsally into adjacent PL and PM. In addition, we studied the histology of the pulvinar using multiple criteria, such as cytoarchitecture and myeloarchitecture; histochemistry for cytochrome oxidase, NADPH-diaphorase, and acetylcholinesterase; and immunocytochemistry for two calcium-binding proteins, calbindin and parvalbumin, and for a neurofilament recognized by the SMI-32 antibody. Some of these stains, mainly calbindin, showed additional subdivisions of the Cebus pulvinar, beyond the traditional PI, PL, and PM. Based on this immunohistochemical staining, the border of PI is moved dorsally above the brachium of the superior colliculus and PI can be subdivided in five regions (PI(P), PI(M), PI(C), PI(L), and PI(LS)). Regions P1, P2, and P3 defined based on efferent connections with cortical visual areas are not architectonically/neurochemically homogeneous. Rather they appear to consist of further chemoarchitectonic subdivisions. These distinct histochemical regions might be related to different functional modules of visual processing within one connectional area.
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PMID:Connectional and neurochemical subdivisions of the pulvinar in Cebus monkeys. 1134 14

The role of basal forebrain corticopetal cholinergic projections in attentional functions has been extensively investigated. For example, 192 IgG-saporin-induced loss of cortical cholinergic inputs was repeatedly demonstrated to result in a selective impairment in the ability of rats to detect signals in a task designed to assess sustained attention performance. The loss of cortical cholinergic inputs correlated highly with the decrease in the hit rate. Little is known about the functions of basal forebrain non-cholinergic neurons, particularly corticopetal GABAergic neurons, largely because of the absence of specific research tools to manipulate selectively this projection. As basal forebrain lesions produced with ibotenic acid were previously observed to potently destroy non-cholinergic, particularly GABAergic neurons while producing only moderate decreases in the density of cortical cholinergic inputs, the present experiment examined the effects of such lesions on sustained attention performance and then compared these effects with the immunohistochemical and attentional consequences of selective cholinotoxic lesions produced by intra-basal forebrain infusions of 192 IgG-saporin. In contrast to the selective decrease in hits previously observed in 192 IgG-saporin-lesioned animals, the attentional performance of ibotenic acid-lesioned animals was characterized by a selective increase in the relative number of false alarms, that is 'claims' for signals in non-signal trials. Analyses of the response latencies suggested that this effect of ibotenic acid was due to impairments in the animals' ability to switch from the processing of the response rules for signal trials to those for non-signal trials. As expected, 192 IgG-saporin did not affect the number of basal forebrain parvalbumin-positive neurons, that are presumably GABAergic, but decreased cortical acetylcholinesterase-positive fiber density by over 80%. Conversely, in ibotenic acid-lesioned animals, basal forebrain parvalbumin-positive cells were decreased by 60% but cortical acetylcholinesterase-positive fiber density was only moderately reduced (less than 25%). These data form the basis for the development of the hypothesis that basal forebrain GABAergic neurons mediate executive aspects of attentional task performance. Such a function may be mediated in parallel via basal forebrain GABAergic projections to the cortex and the subthalamic nucleus.
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PMID:Dissociation between the attentional functions mediated via basal forebrain cholinergic and GABAergic neurons. 1153 Feb 28

The present study describes the cytoarchitectonical and chemoarchitectonical organization of the entorhinal cortex of the mouse (C57BL/6J strain). The entorhinal cortex is medially bordered by the parasubiculum, and laterally by the perirhinal cortex; rostrally and medially it is bordered by the piriform cortex, whereas caudally and dorsally it is bordered by the postrhinal cortex. The entorhinal cortex is divided into two main areas, i.e., the lateral entorhinal area (LEA) and the medial entorhinal area (MEA). Both entorhinal areas are further divided into subfields, i.e., LEA is divided into DLE (dorsolateral entorhinal field), DIE (dorsal intermediate entorhinal field), and VIE (ventral intermediate entorhinal field), whereas MEA is divided into CE (caudal entorhinal field) and ME (medial entorhinal field). Cytoarchitectonically, the main difference between LEA and MEA is displayed by layer II neurons: while these are in a dense layer in LEA, they are more dispersed in MEA. Further, in LEA there is a relatively cell-free zone between layers II and III; this zone is not present in MEA. Histochemically, in acetylcholinesterase (AChE)-stained material, MEA is characterized by darker-stained bands in the superficial layer (i.e., layer I) and in the lamina dissecans, in contrast to LEA, which is more evenly stained for AChE. Further, both the border with the perirhinal cortex and the border with the parasubiculum are characterized by dark-stained bands of AChE. The border between the entorhinal cortex and perirhinal cortex is also easily distinguished in parvalbumin-stained material; while the entorhinal cortex is darkly stained, the perirhinal cortex is lightly stained. In contrast, in sections stained for calretinin, the entorhinal cortex is more lightly stained than the parasubiculum, which has a darkly stained superficial layer, and a densely stained group of neurons in layer III.
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PMID:Entorhinal cortex of the mouse: cytoarchitectonical organization. 1153 Aug 44

There have been previous reports of somatostatin- and acetylcholinesterase (AChE)-positive patches in the superficial layers of the presubiculum in monkeys. In this study, we show additional instances of patches in the presubiculum, as demonstrated by cytochrome oxidase (CO), by myelin and Nissl stains, and by the calcium-binding proteins calbindin (CB), calretinin (CR), and parvalbumin (PV). Markers are differentially expressed along the lateral and longitudinal axes. Comparisons of adjacent sections reacted for different markers suggest that the CB+ and CR+ patches, and CO+ and AChE+ patches generally correspond, but not the CB+ and CO+ patches. In cross section, patches are about 100-300 microm in width. Sections cut tangentially through the superficial layers indicate that the pattern of CO and AChE labeling is in fact patchlike in layer I, but that the apparent patches in layer II (CB and CR) form a reticular or lattice-like network. As patches are restricted to the presubiculum, these labeling patterns provide a convenient marker for the boundary between the presubiculum and the adjoining posteroventral retrosplenial cortex. More work is necessary to determine how this modularity may relate to the functional organization of the presubiculum.
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PMID:Modular organization of the monkey presubiculum. 1154 64

Patients and experimental models of temporal lobe epilepsy display loss of somatostatinergic neurons in the dentate gyrus. To determine if loss of the peptide somatostatin contributes to epileptic seizures we examined kainate-evoked seizures and kindling in somatostatin knockout mice. Somatostatin knockout mice were not observed to experience spontaneous seizures. Timm staining, acetylcholinesterase histochemistry, and immunocytochemistry for NPY, calbindin, calretinin, and parvalbumin revealed no compensatory changes or developmental abnormalities in the dentate gyrus of somatostatin knockout mice. Optical fractionator counting of Nissl-stained hilar neurons showed similar numbers of neurons in wild type and somatostatin knockout mice. Mice were treated systemically with kainic acid to evoke limbic seizures. Somatostatin knockout mice tended to have a shorter average latency to stage 5 seizures, their average maximal behavioral seizure score was higher, and they tended to be more likely to die than controls. In response to kindling by daily electrical stimulation of the perforant path, to more specifically challenge the dentate gyrus, mean afterdischarge duration in somatostatin knockout mice was slightly longer, but the number of treatments to five stage 4-5 seizures was similar to controls. Although we cannot exclude the possibility of undetected compensatory mechanisms in somatostatin knockout mice, these findings suggest that somatostatin may be mildly anticonvulsant, but its loss alone is unlikely to account for seizures in temporal lobe epilepsy.
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PMID:Heightened seizure severity in somatostatin knockout mice. 1182 9


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