| pubmed-article:7617728 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:7617728 | lifeskim:mentions | umls-concept:C0034693 | lld:lifeskim |
| pubmed-article:7617728 | lifeskim:mentions | umls-concept:C1512035 | lld:lifeskim |
| pubmed-article:7617728 | lifeskim:mentions | umls-concept:C0424295 | lld:lifeskim |
| pubmed-article:7617728 | lifeskim:mentions | umls-concept:C0441655 | lld:lifeskim |
| pubmed-article:7617728 | lifeskim:mentions | umls-concept:C1609982 | lld:lifeskim |
| pubmed-article:7617728 | lifeskim:mentions | umls-concept:C1546857 | lld:lifeskim |
| pubmed-article:7617728 | pubmed:issue | 1 | lld:pubmed |
| pubmed-article:7617728 | pubmed:dateCreated | 1995-8-22 | lld:pubmed |
| pubmed-article:7617728 | pubmed:abstractText | Neonatal destruction of mesencephalic dopamine (DA) neurons in rats through administration of 6-hydroxydopamine (6-OHDA; 75 micrograms IC) leads to locomotor hyperactivity at adulthood. Treatment with the catecholamine synthesis inhibitor alpha-methyl-p-tyrosine (H44/68; 250 mg/kg) was shown to reduce the motor activity of neonatally 6-OHDA-lesioned rats to activity levels similar to controls. In both animal groups, DA and metabolite tissue levels decreased after the H44/68 treatment. However, the extent of the H44/68-induced DA decrease was less pronounced in the 6-OHDA-lesioned animals, with no change at all in the dorsal striatum. These results imply that residual activity in mesolimbic DA neurons is required for maintaining the hyperactivity seen after neonatal 6-OHDA lesions, and that this hyperactivity is apparently mediated by postsynaptic alterations. | lld:pubmed |
| pubmed-article:7617728 | pubmed:language | eng | lld:pubmed |
| pubmed-article:7617728 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:7617728 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:7617728 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:7617728 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:7617728 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:7617728 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:7617728 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:7617728 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:7617728 | pubmed:month | May | lld:pubmed |
| pubmed-article:7617728 | pubmed:issn | 0091-3057 | lld:pubmed |
| pubmed-article:7617728 | pubmed:author | pubmed-author:OgrenS OSO | lld:pubmed |
| pubmed-article:7617728 | pubmed:author | pubmed-author:LuthmanJJ | lld:pubmed |
| pubmed-article:7617728 | pubmed:author | pubmed-author:LindqvistEE | lld:pubmed |
| pubmed-article:7617728 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:7617728 | pubmed:volume | 51 | lld:pubmed |
| pubmed-article:7617728 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:7617728 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:7617728 | pubmed:pagination | 159-63 | lld:pubmed |
| pubmed-article:7617728 | pubmed:dateRevised | 2006-11-15 | lld:pubmed |
| pubmed-article:7617728 | pubmed:meshHeading | pubmed-meshheading:7617728-... | lld:pubmed |
| pubmed-article:7617728 | pubmed:meshHeading | pubmed-meshheading:7617728-... | lld:pubmed |
| pubmed-article:7617728 | pubmed:meshHeading | pubmed-meshheading:7617728-... | lld:pubmed |
| pubmed-article:7617728 | pubmed:meshHeading | pubmed-meshheading:7617728-... | lld:pubmed |
| pubmed-article:7617728 | pubmed:meshHeading | pubmed-meshheading:7617728-... | lld:pubmed |
| pubmed-article:7617728 | pubmed:meshHeading | pubmed-meshheading:7617728-... | lld:pubmed |
| pubmed-article:7617728 | pubmed:meshHeading | pubmed-meshheading:7617728-... | lld:pubmed |
| pubmed-article:7617728 | pubmed:meshHeading | pubmed-meshheading:7617728-... | lld:pubmed |
| pubmed-article:7617728 | pubmed:meshHeading | pubmed-meshheading:7617728-... | lld:pubmed |
| pubmed-article:7617728 | pubmed:meshHeading | pubmed-meshheading:7617728-... | lld:pubmed |
| pubmed-article:7617728 | pubmed:meshHeading | pubmed-meshheading:7617728-... | lld:pubmed |
| pubmed-article:7617728 | pubmed:meshHeading | pubmed-meshheading:7617728-... | lld:pubmed |
| pubmed-article:7617728 | pubmed:meshHeading | pubmed-meshheading:7617728-... | lld:pubmed |
| pubmed-article:7617728 | pubmed:meshHeading | pubmed-meshheading:7617728-... | lld:pubmed |
| pubmed-article:7617728 | pubmed:meshHeading | pubmed-meshheading:7617728-... | lld:pubmed |
| pubmed-article:7617728 | pubmed:year | 1995 | lld:pubmed |
| pubmed-article:7617728 | pubmed:articleTitle | Hyperactivity in neonatally dopamine-lesioned rats requires residual activity in mesolimbic dopamine neurons. | lld:pubmed |
| pubmed-article:7617728 | pubmed:affiliation | Preclinical R&D, Astra Arcus AB, Södertälje, Sweden. | lld:pubmed |
| pubmed-article:7617728 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:7617728 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
