| pubmed-article:9842418 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:9842418 | lifeskim:mentions | umls-concept:C0036572 | lld:lifeskim |
| pubmed-article:9842418 | lifeskim:mentions | umls-concept:C0027882 | lld:lifeskim |
| pubmed-article:9842418 | lifeskim:mentions | umls-concept:C1744590 | lld:lifeskim |
| pubmed-article:9842418 | lifeskim:mentions | umls-concept:C0205234 | lld:lifeskim |
| pubmed-article:9842418 | lifeskim:mentions | umls-concept:C0021469 | lld:lifeskim |
| pubmed-article:9842418 | lifeskim:mentions | umls-concept:C1879547 | lld:lifeskim |
| pubmed-article:9842418 | pubmed:issue | 4 | lld:pubmed |
| pubmed-article:9842418 | pubmed:dateCreated | 1999-2-18 | lld:pubmed |
| pubmed-article:9842418 | pubmed:abstractText | The neurons of the thalamic reticular nucleus are among the main targets of corticothalamic projections and their vulnerability in pathological conditions is well established. The present experiments aimed at the description and immunocytochemical characterization of the neurons of the thalamic reticular nucleus activated in neocortical seizures. Focal seizures were induced by the topical application of isotonic, isohydric 4-aminopyridine solution to the sensorimotor neocortex of adult, anesthetized Wistar rats. The animals were perfused with fixative after 1 and 2 h of recorded seizure activity. Coronal plane vibratome sections were incubated with cocktails of polyclonal c-fos and monoclonal parvalbumin antisera. Labeled cells in the thalamic reticular nucleus were counted and related to total cell counts. Neurons and neuropil showed strong parvalbumin immunoreactivity. Double-stained sections revealed that 55.32% of the parvalbumin-positive cell population expressed c-fos protein in their cell nuclei at the end of the 1 h seizure period. This ratio decreased to 43.5% following 2 h seizure. Labeled cells, although less in number were also observed in the contralateral thalamic reticular nucleus. Since parvalbumin labels GABAergic cells, it is tempting to speculate that this activation of intrathalamic inhibiton might exert an important anticonvulsant protection on other thalamic nuclei. | lld:pubmed |
| pubmed-article:9842418 | pubmed:language | eng | lld:pubmed |
| pubmed-article:9842418 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:9842418 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:9842418 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:9842418 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:9842418 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:9842418 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:9842418 | pubmed:month | Nov | lld:pubmed |
| pubmed-article:9842418 | pubmed:issn | 0065-1281 | lld:pubmed |
| pubmed-article:9842418 | pubmed:author | pubmed-author:SzenteMM | lld:pubmed |
| pubmed-article:9842418 | pubmed:author | pubmed-author:DobsAA | lld:pubmed |
| pubmed-article:9842418 | pubmed:author | pubmed-author:PórII | lld:pubmed |
| pubmed-article:9842418 | pubmed:author | pubmed-author:MihályAA | lld:pubmed |
| pubmed-article:9842418 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:9842418 | pubmed:volume | 100 | lld:pubmed |
| pubmed-article:9842418 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:9842418 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:9842418 | pubmed:pagination | 383-93 | lld:pubmed |
| pubmed-article:9842418 | pubmed:dateRevised | 2006-11-15 | lld:pubmed |
| pubmed-article:9842418 | pubmed:meshHeading | pubmed-meshheading:9842418-... | lld:pubmed |
| pubmed-article:9842418 | pubmed:meshHeading | pubmed-meshheading:9842418-... | lld:pubmed |
| pubmed-article:9842418 | pubmed:meshHeading | pubmed-meshheading:9842418-... | lld:pubmed |
| pubmed-article:9842418 | pubmed:meshHeading | pubmed-meshheading:9842418-... | lld:pubmed |
| pubmed-article:9842418 | pubmed:meshHeading | pubmed-meshheading:9842418-... | lld:pubmed |
| pubmed-article:9842418 | pubmed:meshHeading | pubmed-meshheading:9842418-... | lld:pubmed |
| pubmed-article:9842418 | pubmed:meshHeading | pubmed-meshheading:9842418-... | lld:pubmed |
| pubmed-article:9842418 | pubmed:meshHeading | pubmed-meshheading:9842418-... | lld:pubmed |
| pubmed-article:9842418 | pubmed:meshHeading | pubmed-meshheading:9842418-... | lld:pubmed |
| pubmed-article:9842418 | pubmed:meshHeading | pubmed-meshheading:9842418-... | lld:pubmed |
| pubmed-article:9842418 | pubmed:meshHeading | pubmed-meshheading:9842418-... | lld:pubmed |
| pubmed-article:9842418 | pubmed:meshHeading | pubmed-meshheading:9842418-... | lld:pubmed |
| pubmed-article:9842418 | pubmed:meshHeading | pubmed-meshheading:9842418-... | lld:pubmed |
| pubmed-article:9842418 | pubmed:year | 1998 | lld:pubmed |
| pubmed-article:9842418 | pubmed:articleTitle | Early activation of inhibitory neurons in the thalamic reticular nucleus during focal neocortical seizures. | lld:pubmed |
| pubmed-article:9842418 | pubmed:affiliation | Department of Anatomy, Albert Szent-Györgyi Medical University, Szeged, Hungary. | lld:pubmed |
| pubmed-article:9842418 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:9842418 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
