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Query: UNIPROT:P50583 (asymmetrical)
 12,197 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Direct synapses between retinal fibers and neuropeptide Y (NPY) and/or enkephalin-immunoreactive (ENK-I) neurons were investigated in the intergeniculate leaflet (IGL) of the rat, using combined immunohistochemical and degeneration techniques. Degenerating retinal fibers terminated on dendrites of NPY-I and/or ENK-I neurons. NPY-I fibers in the IGL formed axo-dendritic synapses on non-immunoreactive dendrites. Most of them were asymmetrical synapses. ENK-I axon terminals contacted non-immunoreactive dendrites with symmetrical synapse.
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PMID:Retinal fibers make synaptic contact with neuropeptide Y and enkephalin immunoreactive neurons in the intergeniculate leaflet of the rat. 185 61

In the chicken, serotonin-immunoreactive cells were widely distributed not only in the carotid body but also in the wall of the common carotid artery and around each artery arising from the common carotid artery. Almost all of the serotonin cells in the wall of the common carotid artery were intensely immunoreactive to the neuropeptide Y, met- and leu-enkephalin antisera, whereas in the carotid body only a few cells were immunoreactive to these antisera. Innervation of the serotonin cells in and around arteries of chickens was investigated by immunohistochemistry and electron microscopy, in comparison with that of the carotid body. The serotonin cell groups in and around arteries, as well as the carotid body, received numerous peptidergic nerve fibers. Calcitonin gene-related peptide (CGRP)- and substance P-immunoreactive varicose nerve fibers were densely distributed, and somatostatin-immunoreactive fibers were moderately distributed in the serotonin cell groups. Galanin- and vasoactive intestinal peptide (VIP)-immunoreactive fibers were sparsely distributed in the cell groups. By electron microscopy, the serotonin cells in and around arteries were characterized by the presence of numerous dense-cored vesicles, 70-220 nm in diameter. The granule-containing cells were in close association with numerous axons. Naked axons regarded axon terminals were frequently apposed on the granular cells. The axon terminals were usually long and often partly invested the granular cells. Numerous synaptic junctions were detected along the contact between the granular cells and axon terminals. Most of the synaptic junctions showed afferent morphology; the secretory granules were accumulated near and attached to the asymmetrical membrane thickenings. Thus, the serotonin cells in and around arteries, like the carotid body, constitute chemoreceptive tissue.
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PMID:Innervation of the serotonin-immunoreactive cells distributed in the wall of the common carotid artery and its branches in the chicken. 232 11

In the present study, we examined the ultrastructure of striatal neurons containing neuropeptide Y (NPY) which were labeled by an immunohistochemical method using peroxidase-conjugated F(ab) fragments in the rat. Each of the 26 neurons identified had a deeply indented oval nucleus. The cytoplasm, which was mainly concentrated at the emergence of the dendrites, contained an abundant Golgi apparatus and a well-developed granular endoplasmic reticulum. Dendrites were poorly branched and rarely exhibited varicosities or dendritic spines. NPY-immunoreactive (Ir) axons were small in diameter and unmyelinated. These features corresponded to a subpopulation of striatal neurons classified as aspiny type IV in previous Golgi studies. Axon terminals forming symmetrical synapses were numerous on the NPY-Ir perikarya and proximal dendrites. On distal NPY-Ir dendrites, synaptic contacts were mainly of the asymmetrical type, suggesting that NPY neurons are contacted by at least 2 categories of afferent fibers. Several NPY-Ir axonal processes and boutons were found to form symmetrical synapses with dendrites, dendritic spines and perikarya belonging to spiny type neurons. These data were consistent with the view that NPY may act as a neurotransmitter of striatal interneurons. Moreover, the frequent observation of NPY axonal processes in the close vicinity of striatal vessels suggested that NPY might also play a role in the control of cerebral vasomotricity. Thirty hours after intranigral injection of 6-hydroxydopamine to induce a degeneration of nigrostriatal dopamine terminals, some characteristic degenerative boutons were observed in close apposition to NPY-Ir cell bodies, suggesting that NPY neurons are under a direct nigrostriatal dopaminergic influence.
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PMID:Ultrastructural features of NPY-containing neurons in the rat striatum. 270 86

This study examines the ultrastructural relationships established by the nigrostriatal dopaminergic and the corticostriatal afferent fibers with neuropeptide Y (NPY)-containing neurons in the rat striatum. By means of dual immunolabeling procedures using peroxidase conjugated F(ab) fragments and 125I-labeled protein A, direct appositions and morphologically defined synaptic contacts of the symmetrical type were visualized between tyrosine hydroxylase-labeled nerve terminals and NPY-labeled neurons. After deafferentation of the striatum from its cortical input direct appositions and asymmetrical synaptic contacts were evidenced between characteristic degenerative boutons and NPY-positive neurons in the striatum. These results suggest that striatal NPY interneurons undergo direct influence from both nigrostriatal dopaminergic and corticostriatal neuronal systems.
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PMID:Ultrastructural correlates of functional relationships between nigral dopaminergic or cortical afferent fibers and neuropeptide Y-containing neurons in the rat striatum. 276 90

We have proposed recently that a pertussistoxin-insensitive Ca2+ influx stimulated by Y2-type receptor activation in CHP-234 human neuroblastoma cells underlies increases in intracellular free Ca2+ concentration ([Ca2+]i) induced by neuropeptide Y (NPY), which were strictly dependent on extracellular Ca2+ and independent of internal Ca2+ stores. We describe here the actions of NPY in these same cells, using the activity of Ca(2+)-activated K+ channels as an indicator of [Ca2+]i. The elementary slope conductance of these channels was 110 +/- 3 pS (with an asymmetrical K+ gradient), their activity was greatly increased by application of ionomycin, and they were reversibly blocked by 1 mM tetraethylammonium (TEA) and 100 nM charybdotoxin. Application of 100 nM NPY, in the presence but not in the absence of extracellular Ca2+, increased the channel open probability. ATP applied in the absence of external Ca2+ caused rises both in channel open probability and [Ca2+]i. Inositol trisphosphate production was stimulated by ATP but not by NPY. In outside-out patches, NPY increased channel open probability, indicating that NPY-associated Ca2+ influx does not require all the intracellular machinery present in intact cells. Channel activation by NPY was unaffected by the replacement of guanosine 5'-triphosphate (GTP) by (guanosine 5'-O-(2-thiodiphosphate) (GDP[ beta S]), a non-hydrolysable GDP analogue, in the pipette internal solution, consistent with the lack of involvement of G-proteins in the coupling of Y2-type receptors to Ca2+ influx in CHP-234 cells.
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PMID:Neuropeptide Y2-type receptor-mediated activation of large-conductance Ca(2+)-sensitive K+ channels in a human neuroblastoma cell line. 749 Dec 80

Hilar mossy cells of the mouse were shown recently to display calretinin immunoreactivity (Liu et al. [1996] Exp Brain Res 108:389-403). The morphological and connectional characteristics of these cells are poorly understood. In the present study, we used immunohistochemical, electron microscopic, and neuronal tracing techniques to describe their distribution, morphology, and connectivity. The distribution of calretinin-immunoreactive mossy cells varied significantly along the dorsoventral axis of the hilus. At dorsal levels, calretinin immunoreactivity was limited largely to a subpopulation of interneurons. At mid-dorsoventral and ventral levels, however, most if not all mossy cells displayed calretinin immunoreactivity. We found that most hilar mossy cells are calretinin immunoreactive but lack gamma-aminobutyric acid, as demonstrated by postembedding immunostaining of alternate semithin sections. Calretinin-immunoreactive mossy cells typically had two to three thick dendrites covered with complex spines (thorny excrescences). Electron microscopy revealed that these spines received multiple asymmetric contacts from mossy fibres. Axons arising from these cells formed a strong belt of calretinin immunoreactivity restricted to the inner third of the dentate molecular layer. This immunoreactivity was equally dense throughout the dorsoventral length of the dentate gyrus, suggesting that axons of calretinin-immunoreactive mossy cells located in the ventral levels diverge greatly and are capable of innervating distant regions of the dentate gyrus. Ultrastructural examination showed that calretinin-immunoreactive boutons made asymmetric synaptic contacts primarily on spines and, occasionally, on dendritic shafts of granule cells and accounted for the majority of asymmetrical synapses in the inner molecular layer. Injections of the retrograde tracer wheatgerm agglutinin-gold into the dentate gyrus demonstrated that calretinin-immunoreactive mossy cells concentrated in the ventral hilus project massively to both the dorsal and ventral aspect of the contralateral dentate gyrus. A small proportion of retrogradely labelled cells showed immunoreactivity for neuropeptide Y or somatostatin. If mossy cells of the ventral hilus receive the majority of their input from ventral granule cells, one may expect ventral granule cells to be more efficient in recruiting large numbers of granule cells during synchronous activity patterns than dorsal granule cells. Spontaneous activity originating from granule cells in the ventral dentate gyrus can be propagated throughout the dorsoventral length of the dentate gyrus bilaterally via the dorsoventrally divergent and contralaterally projecting axons of the mossy cells. This organization may explain why the ventral dentate gyrus is frequently involved in pathological phenomena.
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PMID:Distribution, ultrastructure, and connectivity of calretinin-immunoreactive mossy cells of the mouse dentate gyrus. 922 28

The present study determined the effects of intraventricularly administered glial cell line-derived neurotrophic factor on the behavioral and neurochemical sequelae of unilateral excitotoxic lesions of the striatum. Distinct asymmetrical rotational behavior in response to peripheral administration of amphetamine (5 mg/kg) was noted one and two weeks following injections of quinolinic acid (200 nmol) into two sites in the left striatum. In rats given a single intraventricular injection of glial cell line-derived neurotrophic factor (10-1000 micrograms) 30 min before the toxin, amphetamine-induced rotational behavior was significantly attenuated. Analysis of Nissl-stained coronal sections showed marked neuronal loss in the striatum ipsilateral to the quinolinic acid injections, which was at least partially prevented by glial cell line-derived neurotrophic factor D1 and D2 dopamine binding sites in the striatum, the majority of which are localized to subpopulations of GABAergic neurons, were decreased to a similar extent by quinolinic acid. Moreover, the reduction was attenuated by glial cell line-derived neurotrophic factor treatment to a similar degree, suggesting that the two subpopulations of GABAergic striatal output neurons are equally vulnerable to excitotoxic damage. Concomitant changes in neurotransmitter function as a result of the lesion were also observed: [3H]GABA uptake into striatal target tissues (globus pallidus and substantia nigra) was considerably reduced in the lesioned compared to the contralateral unlesioned tissues, as were [3H]choline and [3H]dopamine uptake into striatal synaptosomes. Similarly, striatal choline acetyltransferase activity was decreased by the lesion. Decrements in neuropeptide levels of similar magnitude were evident ipsilateral to the lesion; substance P, met-enkephalin and dynorphin A contents in the globus pallidus and substantia nigra were significantly reduced. Striatal somatostatin and neuropeptide Y levels were not altered. All of the neurochemical deficits induced by striatal quinolinic acid lesions were attenuated by intraventricular delivery of glial cell line-derived neurotrophic factor. Continuous intraventricular infusion of this trophic factor (10 micrograms/day) over a two-week period did not afford notable improvement compared to the single injection of 10 micrograms. In contrast, continuous infusion of brain-derived neurotrophic factor (10 micrograms/day) directly into the striatum did not affect any of the neurochemical parameters studied. However, neurotrophin-3 (10 micrograms/day) delivery into the striatum significantly increased [3H]GABA uptake, but only modestly affected [3H]choline uptake. The results indicate that glial cell line-derived neurotrophic factor counteracts neuronal damage induced by a striatal excitotoxic insult and support its potential use as a treatment for central nervous system disorders that may be a consequence of excitotoxic processes, such as Huntington's disease.
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PMID:Glial cell line-derived neurotrophic factor attenuates the excitotoxin-induced behavioral and neurochemical deficits in a rodent model of Huntington's disease. 933 Mar 71

This study examined the effects of unilateral thermocoagulatory cortical lesion on the pattern of neuropeptide Y immunostaining in the rat ipsilateral striatum at 4 and 21 days post-lesion. Light microscopic analysis showed a significant increase in the number of neuropeptide Y-positive neurons vs. control at both time points; paradoxically, the intraneuronal level of labelling significantly decreased at 4 days post-lesion but increased at 21 days post-lesion. Ultrastructural analysis in control condition showed a higher proportion of dendritic versus axonal labelled processes (3.5 ratio); all the neuropeptide Y synaptic terminals formed symmetrical contacts, mostly onto unlabelled dendrites. At 4 days post-lesion, the neuropeptide Y-positive axon density dramatically increased (+576%) without significant change in the labelled dendrite density, vs. control values; the density of neuropeptide Y synaptic terminals increased in parallel by 233%. In addition, a significant proportion of large neuropeptide Y boutons forming asymmetrical synapses onto unlabelled spines were observed. At 21 days post-lesion, densities of neuropeptide Y dendrites, axons, and synaptic terminals increased by 68, 246 and 125%, respectively, vs. control. But, the morphological features of the neuropeptide Y axonal processes and synaptic specializations of the boutons were similar to those observed in control condition. These data (1) raise an important issue regarding the origin of the terminals forming asymmetrical synapses in the striatum, (2) suggest that adaptative changes in the neuropeptide Y neuronal network may be a main component of striatal remodelling resulting from the progressive loss of cortical inputs, and (3) reinforce the view that neuropeptide Y and excitatory amino acid functions may be tightly linked in the striatum.
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PMID:Ultrastructural and metabolic changes in the neuropeptide Y-containing striatal neuronal network after thermocoagulatory cortical lesion in adult rat. 1052 58