pubmed-article:8095700 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:8095700 | lifeskim:mentions | umls-concept:C0004927 | lld:lifeskim |
pubmed-article:8095700 | lifeskim:mentions | umls-concept:C1280500 | lld:lifeskim |
pubmed-article:8095700 | lifeskim:mentions | umls-concept:C1555903 | lld:lifeskim |
pubmed-article:8095700 | lifeskim:mentions | umls-concept:C0524474 | lld:lifeskim |
pubmed-article:8095700 | pubmed:issue | 1 | lld:pubmed |
pubmed-article:8095700 | pubmed:dateCreated | 1993-4-12 | lld:pubmed |
pubmed-article:8095700 | pubmed:abstractText | Aged rats were chronically administered acetyl-L-carnitine (AC) for 10 months. During this period they were tested on learning and sensorimotor tasks and were then subsequently tested electrophysiologically to assess induction and decay rates of long-term synaptic enhancement (LTE) in the hippocampus. Four groups were tested: young controls (4 mo-con), middle-aged controls (16 mo-con), old controls (24 mo-con), and old AC-treated rats (24 mo-AC). After completion of electrophysiological testing, each rat was sacrificed and investigated for age- or drug-related changes in three neurotransmitter markers; including, NMDA-sensitive glutamate receptors, high affinity choline uptake, and adenosine receptor number in the neocortex, hippocampus or caudate nucleus. Aging impaired spatial learning and there was a robust positive correlation between NMDA receptors in the hippocampus and acquisition of the spatial learning task. Induction of hippocampal LTE was reduced in 24 mo-AC rats and NMDA receptor number and high-affinity choline uptake in the frontal cortex was increased. Several suggestions are offered to explain the action of AC on these neurobiological parameters in old rats. | lld:pubmed |
pubmed-article:8095700 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:8095700 | pubmed:language | eng | lld:pubmed |
pubmed-article:8095700 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:8095700 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:8095700 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:8095700 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:8095700 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:8095700 | pubmed:issn | 0197-4580 | lld:pubmed |
pubmed-article:8095700 | pubmed:author | pubmed-author:DavisSS | lld:pubmed |
pubmed-article:8095700 | pubmed:author | pubmed-author:BarnesC ACA | lld:pubmed |
pubmed-article:8095700 | pubmed:author | pubmed-author:WangK PKP | lld:pubmed |
pubmed-article:8095700 | pubmed:author | pubmed-author:MarkowskaA... | lld:pubmed |
pubmed-article:8095700 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:8095700 | pubmed:volume | 14 | lld:pubmed |
pubmed-article:8095700 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:8095700 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:8095700 | pubmed:pagination | 107-15 | lld:pubmed |
pubmed-article:8095700 | pubmed:dateRevised | 2007-11-14 | lld:pubmed |
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pubmed-article:8095700 | pubmed:articleTitle | Acetyl-L-carnitine: behavioral, electrophysiological, and neurochemical effects. | lld:pubmed |
pubmed-article:8095700 | pubmed:affiliation | Arizona Research Laboratories, University of Arizona, Tucson 85724. | lld:pubmed |
pubmed-article:8095700 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:8095700 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
pubmed-article:8095700 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:8095700 | lld:pubmed |
http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:8095700 | lld:pubmed |