Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C1519176 (PSA)
 5,490 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Using the model of lysolecithin-induced demyelination of the corpus callosum in wild-type, NCAM-deficient, and endoneuraminidase-injected mice, we have analyzed the consequences of the loss of expression of NCAM or PSA residues on the migration and proliferation capacities of neural precursors of the subventricular zone (SVZ). We showed that the absence of PSA or NCAM delayed migration of neural precursors to the olfactory bulb and consequently enhanced their recruitment at the lesion site. Moreover, after demyelination, the lack of NCAM but not PSA promoted proliferation in the SVZ and the lesion while the lack of PSA favored the differentiation of the traced cells into the oligodendroglial fate both in the SVZ and in the lesion. As previously demonstrated in vitro (L. Decker et al., 2000, Mol. Cell. Neurosci. 16, 422-439), these data illustrate the involvement of PSA and NCAM in neural precursor motility and differentiation in the normal and injured central nervous system, suggesting distinct roles for these two molecules under pathophysiological conditions.
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PMID:Loss of polysialic residues accelerates CNS neural precursor differentiation in pathological conditions. 1186 Feb 75

The polysialylated form of the neural cell adhesion molecule (PSA-NCAM) continues to be expressed in the adult hippocampus, mainly in a subset of neurons located in the innermost portion of the granule cell layer. PSA-NCAM immunoreactive neurons have also been described outside this layer in humans, where they are severely reduced in schizophrenic brains. Given this important clinical implication, we were interested in finding whether similar neurons existed in the adult rat hippocampus and to characterize their distribution, morphology and phenotype. PSA-NCAM immunocytochemistry reveals labeled neurons in the subiculum, fimbria, alveus, hilus, and stratum oriens, lucidum and radiatum of CA3 and CA1. They are mainly distributed in the ventral hippocampus, and have polygonal or fusiform somata with multipolar or bipolar morphology. These neurons show long straight dendrites, which reach several strata and even enter the fimbria and the alveus. These dendrites are often varicose, appear devoid of excrescences and apparently do not show spines. Most of these neurons display GABA immunoreactivity and further analysis has shown that a subpopulation expresses calretinin, but not somatostatin, neuropeptide Y, parvalbumin, calbindin or NADPH diaphorase. Our study demonstrates that there is an important subpopulation of PSA-NCAM immunoreactive neurons, many of which can be considered interneurons, outside the rat granule cell layer, probably homologous to those described in the human hippocampus. The presence of the polysialylated form of NCAM in these neurons could indicate that they are undergoing continuous remodeling during adulthood and may have an important role in hippocampal structural plasticity.
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PMID:Non-granule PSA-NCAM immunoreactive neurons in the rat hippocampus. 1187 89

The stage of neurogenesis can be divided into three steps: proliferation, migration, and differentiation. To elucidate detailed relations between these three steps after ischemia, the authors evaluated the three steps in the adult gerbil dentate gyrus (DG) after 5 minutes of transient global ischemia using bromodeoxyuridine (BrdU), highly polysialylated neural cell adhesion molecule (PSA-NCAM), and neuronal nuclear antigen (NeuN) and glial fibrillary acidic protein (GFAP) as markers for proliferation, migration, and differentiation, respectively. Bromodeoxyuridine-labeled cells increased approximately sevenfold, and PSA-NCAM-positive cells increased approximately threefold in the subgranular zone (SGZ) with a peak 10 days after ischemia. Bromodeoxyuridine-labeled cells with PSA-NCAM expression were first detected both in the SGZ and the granule cell layer (GCL) 20 days after ischemia and gradually decreased after that, whereas BrdU-labeled cells with NeuN gradually increased in the GCL until 60 days after ischemia. A few BrdU-labeled cells with GFAP expression were detected in DG after ischemia; no PSA-NCAM-positive cells with GFAP expression were detected, but the radial processes of glial cells were partly in contact with PSA-NCAM-positive cell bodies and dendrites. These results suggest that neural stem cell proliferation begins at the SGZ, and that the cells then migrate into the GCL and differentiate mainly into neuronal cells. The majority of these three steps finished in 2 months after transient global ischemia.
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PMID:Three steps of neural stem cells development in gerbil dentate gyrus after transient ischemia. 1191 12

Immunoreactive highly polysialylated neural cell adhesion molecule (PSA-NCAM) expression was examined in the rat with repeated exposure to amygdaloid kindled generalized seizures (GS). In the sham control brain, PSA-NCAM staining was slightly observed in the subventricular zone (SVZ) of the striatum. The number of PSA-NCAM positive cells increased four times in the bilateral SVZ after three consecutive GS, with a further increase after 30 consecutive GS. As PSA-NCAM is involved in neural plasticity as well as migration of neural stem cells (NSC), expression of PSA-NCAM in the SVZ suggests that the recurrent GS may mainly contribute to reconstruction of synaptic network and could also contribute to NSC migration after kindling.
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PMID:Expression of highly polysialylated neural cell adhesion molecule in rat subventricular zone with exposure to repeated kindled seizures. 1195 29

In the adult central nervous system, the expression of polysialylated forms of the cell-surface glycoprotein NCAM (PSA-NCAM) is thought to be confined to areas particularly susceptible to plastic changes. In the present study, PSA-NCAM was found to be expressed in the somata, dendrites and axonal processes of some neurons, including cartridge-like elements, which according to our criteria, were identified as chandelier cell axon terminals (chandelier terminals), in the adult human entorhinal cortex and neocortex. These chandelier terminals were very numerous in layers II and III, whereas in deeper layers they were found only occasionally. Double immunocytochemical staining for PSA-NCAM with parvalbumin (PV), with GABA transporter (GAT-1) or with the 5-HT(1A) serotonin receptor allowed us to verify them as true chandelier terminals. Nearly all (92-95%) PV-immunoreactive (-ir) and GAT-1-ir chandelier terminals in layers II and III coexpressed PSA-NCAM. Most of the PSA-NCAM-ir chandelier terminals (89-98%) were also labeled for PV and GAT-1. The results suggest that chandelier terminals in layers II and III of the human entorhinal cortex and temporal neocortex might be particularly susceptible to plastic changes.
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PMID:PSA-NCAM immunoreactivity in chandelier cell axon terminals of the human temporal cortex. 1200 61

The polysialylated, embryonic form of the neuronal cell adhesion molecule (PSA-NCAM) is known to participate in a whole series of synaptic rearrangements even in adult animals. The possible role of this molecule in neuroplastic changes of the adult rat somatosensory cortex induced by unilateral transection of the infraorbital branch of the trigeminal nerve was studied with PSA-NCAM immunostaining at light microscopic level. Two- and three-month-old CFY albino rats were sacrificied on days 1, 4, 6, 14 and 21 following operation and PSA-NCAM immunoreaction was examined at three levels of the vibrissa-cortex neuraxis, namely, in the principal nucleus of the trigeminal nerve, in the ventral posteromedial nucleus of the thalamus and in the somatosensory cortex. The lower levels of the neuraxis remained free of PSA-NCAM labeling, similarly to control, intact animals. However, a large number of scattered small neurons became PSA-NCAM immunoreactive in layers IV-VI on both ipsi- and contralateral sides of the somatosensory cortex from day 6 onwards, suggesting a possible transynaptic regulation of NCAM sialylation state.
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PMID:Transneuronal induction of the highly sialylated isoform of the neural cell adhesion molecule following nerve injury. 1206 80

Highly polysialylated neural cell adhesion molecules (PSA-NCAMs) are involved in migration of neural stem cells as well as neural plasticity. Immunoreactive PSA-NCAM expression was examined in rat with repeated exposure to amygdaloid kindled generalized seizures (GS). The number of PSA-NCAM positive cells in bilateral dentate gyrus (DG) increased significantly at GS. Although total positive cell number was not significantly different between 3 times GS (3 GS) and 30 times GS (30 GS) groups, a greater number of positive cells was located in the outer granule cell layer (GCL), and the immunopositive dendrite greatly extended to the molecular layer in the 30 GS group. These observations indicate that increased migration of newly generated cells as well as plastic change of originally-existed neural cells may occur in response to the recurrent GS, which may contribute to abnormal reconstruction of synaptic network in hippocampus and epileptogenisity in kindling.
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PMID:Changes of localization of highly polysialylated neural cell adhesion molecule (PSA-NCAM) in rat hippocampus with exposure to repeated kindled seizures. 1213 37

Synaptic plasticity in the amygdala appears to be necessary for the generation of emotional memories. However, the molecular bases of this plasticity are not fully understood. Because the polysialylated form of the neural cell adhesion molecule (PSA-NCAM) has been implicated in memory consolidation in the hippocampus and temporal cortex, we have studied in detail the expression of this molecule in the adult rat amygdala with an antibody against PSA-NCAM. Our results demonstrate for the first time the presence of PSA-NCAM in the adult rat amygdala. Immunoreactive somata and processes are abundant in the amygdalo-hippocampal transition area, central nucleus, intra-amygdaloid bed nucleus of the stria terminalis, anterior and posterior cortical nuclei, periamygdaloid cortex and medial nucleus of the amygdala. In addition PSA-NCAM immunoreactive neuronal somata and processes exist in the lateral, basal and accessory basal nuclei, anterior amygdaloid area and amygdalo-striatal area. The presence of this molecule in areas that receive olfactory or vomeronasal input could reflect the intrinsic plasticity of these chemosensory systems. PSA-NCAM expression in the lateral amygdala could indicate its participation in the plastic events that lead to the generation of emotional memories such as those related to fear conditioning.
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PMID:Distribution of PSA-NCAM expression in the amygdala of the adult rat. 1215 Jul 68

Multiple sclerosis is affecting approximately 1 out of every 1000 individuals in the western world. After axons are denuded of myelin in the early stages of the disease, remyelination occurs, but eventually this process fails, and permanent disability is the result. During development, the polysialylated form of the neural cell adhesion molecule NCAM, PSA-NCAM, is expressed at the axonal surface and acts as a negative regulator of myelination, presumably by preventing myelin-forming cells from attaching to the axon. Removal of PSA-NCAM from the axonal surface is a prerequisite for the initiation of myelination. We questioned whether, in multiple sclerosis, re-expression of PSA-NCAM by axons could occur, and therefore account for the failure of remyelination. Forty multiple sclerosis lesions from 24 different post-mortem multiple sclerosis cases were selected by histological methods and analysed by immunohistochemistry. Demyelinated lesions and partially remyelinated lesions (shadow plaques) were studied. Controls consisted of post-mortem brain tissue from patients with amyotrophic lateral sclerosis and without neurological disease. We showed that PSA-NCAM, normally absent from adult brain, is re-expressed on demyelinated axons in the plaques. Within shadow plaques, remyelinated axons do not express PSA-NCAM. Re-expression of PSA-NCAM could act as an inhibitor of remyelination and participate in disease progression in multiple sclerosis.
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PMID:Re-expression of PSA-NCAM by demyelinated axons: an inhibitor of remyelination in multiple sclerosis? 1218 43

Neural stem cells (NSCs) were isolated from embryonic day 16 Sprague-Dawley rats and cultured in a novel serum-free stem cell medium that selected for the growth of NSCs and against the growth of GFAP(+) cells (astrocytes). NSCs maintained in culture for extended periods of time retained immunoreactivity for both nestin and PSA-NCAM, two markers characteristic of the stem cell phenotype. Moreover, using an oligodendrocyte (OL) specification medium, NSCs differentiated into OL as evidenced by their morphology and expression of multiple oligodendrocyte/myelin-specific markers. In addition, NSCs are capable of acquiring a neuronal phenotype as evidenced by expressing neuronal markers, such as neurofilament (NF) and NeuN when cultured in a defined medium for neurons indicating that these cells are also a good source of neuroblasts, which could be used to replace neuronal populations in the brain. We also showed successful propagation and differentiation of NSCs into OL after cryostorage, allowing for the later use of stored NSCs. The long-term goal of culturing NSCs and committed oligodendrocyte progenitors (OLP) is to obtain homogeneous populations for transplantation with the goal of remyelinating the myelin-deficient CNS. Our preliminary experiments carried out on normal and myelin deficient rats demonstrate that these cells survive and migrate extensively in both types of hosts. NSCs grafted as such, as well as cells derived from NSCs exposed to selective specification before grafting, are able to differentiate within the host brain. As expected, NSCs are capable of giving rise to astrocytes in a medium favoring this phenotype.
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PMID:Selective specification of CNS stem cells into oligodendroglial or neuronal cell lineage: cell culture and transplant studies. 1220 75


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