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)

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

Impairment of GABA-mediated inhibition is one of the main hypotheses invoked to explain seizure activity, both in experimental models and in human epilepsy. We have studied the distribution and the neurochemical characteristics of certain GABAergic circuits in the normal and epileptic human sclerotic hippocampal formation. We have focused our attention mainly on chandelier cells because, together with basket cells, they are considered to have powerful effects on spike generation. Chandelier cells represent a unique type of interneuron whose axon terminals (Ch-terminals) form synapses with the axon initial segments of cortical pyramidal cells and granular cells of the dentate gyrus. Different neurochemical subpopulations of chandelier cells have been identified by immunocytochemistry, mainly in the neocortex. Markers for Ch-terminals include the GABA transporter 1 (GAT-1), the polysialylated form of the cell-surface glycoprotein neural cell adhesion molecule (PSA-NCAM) and the calcium-binding proteins parvalbumin (PV) and calbindin D-28k (CB). In the normal hippocampal formation, GAT-1- and PV-immunoreactive (-ir) Ch-terminals were identified in the granular and polymorphic layers of the dentate gyrus, in the strata pyramidale and oriens of the CA fields, and in the pyramidal layer of the subicular complex. In addition, and in contrast to the hippocampus and dentate gyrus, subsets of Ch-terminals in the upper pyramidal layer of the normal subiculum express CB and PSA-NCAM. The sclerotic hippocampus of epileptic patients presented an impressive morphological and neurochemical reorganization of Ch-terminals and basket formations. This was apparent in the dentate gyrus and hippocampal formation, but not in the subiculum, which appeared to remain unaltered. Principally, numerous and more complex PV- and CB-ir Ch-terminals, as well as dense PV-ir basket formations, appeared in some hippocampal segments, whereas in other regions there was a lack of labelled elements. These changes varied considerably not only between different patients, but also within different hippocampal fields in a given patient. In general, the changes were not correlated with the clinical characteristics or degree of histopathological alterations observed in the patients, such as granular cell dispersion, neuron loss and proliferation of mossy fibres. However, some surviving neurons in the regions adjacent to the areas of neuron loss were consistently innervated by dense basket formations and complex Ch-terminals. These results indicate that, in the human epileptic hippocampus, GABAergic circuits are more highly modified than previously thought. When considered along with other extrahippocampal alterations, we suggest that these changes are important in the pathophysiology of temporal lobe epilepsy associated with hippocampal sclerosis.
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PMID:Histopathology and reorganization of chandelier cells in the human epileptic sclerotic hippocampus. 1453 59

Chandelier neurons and their characteristic arrays of axonal terminals, known as cartridges, have been implicated in a variety of psychiatric and neurological disorders including schizophrenia and epilepsy. As a result, these neurons have been extensively examined in the brains of several species using a range of markers. However, these markers have not been systematically compared in a single species for their robustness in labelling chandelier cell cartridges. We have therefore examined several markers, reported to label chandelier arrays in primates, for their capacity to mark these structures in rat medial prefrontal cortex and hippocampus. These studies revealed that cartridge-like structures were labelled by parvalbumin and GAT-1 immunohistochemistry in both medial prefrontal cortex and hippocampus of the rat brain. Additionally, GAD65 immunohistochemistry labelled array-like structures preferentially in the dentate gyrus. In contrast, PSA-NCAM, calbindin and GAD67 immunohistochemistry did not reveal any array-like structures in either region of rat brain. These observations indicate that the various immunological markers previously used to visualise chandelier cell cartridges in primates are not equally efficient in labelling these structures in the rat brain, and that GAT-1 immunohistochemistry is the most robust means of visualising chandelier cell cartridges in the regions examined. These are important considerations for quantitative studies in animal models of neurological disorders where chandelier neurons are implicated.
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PMID:A comparison of possible markers for chandelier cartridges in rat medial prefrontal cortex and hippocampus. 1564 49

The polysialylated form of the neural cell adhesion molecule (PSA-NCAM) is involved in several morphogenetic processes of the central nervous system. In the present study the expression of PSA-NCAM has been investigated in the rat thalamus during embryonic and postnatal development using light and electron microscopic immunocytochemical techniques. At all the examined ages, PSA-NCAM staining in the thalamus was mainly observed along neuronal plasmatic membranes and absent in astrocytes identified by labelling with cytoskeletal (vimentin and glial fibrillary acidic protein) and membrane (GABA transporter-3) markers. At embryonic day 14 the immunoreactivity was restricted to the dorsal thalamic mantle and to the region of reticular thalamic migration and subsequently it extended throughout the whole thalamic primordium. PSA-NCAM labelling remained intense and homogeneously distributed along perinatal period, but from P4 it began to decrease selectively, persisting throughout adulthood only in the reticular nucleus, ventral lateral geniculate nucleus and midline and intralaminar nuclei. The expression of this adhesion molecule differed in areas characterized by the presence of neurons containing distinct calcium binding proteins, as PSA-NCAM labelling was intense around calretinin-positive neurons, whereas it decreased in some calbindin-immunoreactive regions. These findings show evidence of a selective neuronal expression of PSA-NCAM in developing thalamus, supporting its suggested role in cell migration and synaptogenesis as it occurs in the cerebral cortex. In adulthood PSA-NCAM could instead be a marker of thalamic nuclei that retain a potential for synaptic plasticity.
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PMID:PSA-NCAM in the developing and mature thalamus. 1729