pubmed-article:2346619 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:2346619 | lifeskim:mentions | umls-concept:C0034493 | lld:lifeskim |
pubmed-article:2346619 | lifeskim:mentions | umls-concept:C0009647 | lld:lifeskim |
pubmed-article:2346619 | lifeskim:mentions | umls-concept:C1552622 | lld:lifeskim |
pubmed-article:2346619 | pubmed:issue | 2 | lld:pubmed |
pubmed-article:2346619 | pubmed:dateCreated | 1990-7-12 | lld:pubmed |
pubmed-article:2346619 | pubmed:abstractText | The role of the hippocampus (HPC) in trace eye-blink conditioning was evaluated using a 100-ms tone conditioned stimulus (CS), a 300- or 500-ms trace interval, and a 150-ms air puff unconditioned stimulus (UCS). Rabbits received complete hippocampectomy (dorsal & ventral), sham lesions, or neocortical lesions. Hippocampectomy produced differential effects in relation to the trace interval used. With a 300-ms trace interval, HPC-lesioned Ss showed profound resistance to extinction after acquisition. With a 500-ms trace interval, HPC-lesioned Ss did not learn the task (only 22% conditioned responses (CRs) after 25 sessions, whereas controls showed greater than 80% after 10 sessions), and on the few trials in which a CR occurred, most were "nonadaptive" short-latency CRs (i.e., they started during or just after the CS and always terminated prior to UCS onset). The authors conclude that the HPC encodes a temporal relationship between CS and UCS, and when the trace interval is long enough (e.g., 500 ms), that the HPC is necessary for associative learning of the conditioned eye-blink response. | lld:pubmed |
pubmed-article:2346619 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:2346619 | pubmed:language | eng | lld:pubmed |
pubmed-article:2346619 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:2346619 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:2346619 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:2346619 | pubmed:month | Apr | lld:pubmed |
pubmed-article:2346619 | pubmed:issn | 0735-7044 | lld:pubmed |
pubmed-article:2346619 | pubmed:author | pubmed-author:DisterhoftJ... | lld:pubmed |
pubmed-article:2346619 | pubmed:author | pubmed-author:DeyoR ARA | lld:pubmed |
pubmed-article:2346619 | pubmed:author | pubmed-author:MoyerJ RJRJr | lld:pubmed |
pubmed-article:2346619 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:2346619 | pubmed:volume | 104 | lld:pubmed |
pubmed-article:2346619 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:2346619 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:2346619 | pubmed:pagination | 243-52 | lld:pubmed |
pubmed-article:2346619 | pubmed:dateRevised | 2007-11-14 | lld:pubmed |
pubmed-article:2346619 | pubmed:meshHeading | pubmed-meshheading:2346619-... | lld:pubmed |
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pubmed-article:2346619 | pubmed:meshHeading | pubmed-meshheading:2346619-... | lld:pubmed |
pubmed-article:2346619 | pubmed:year | 1990 | lld:pubmed |
pubmed-article:2346619 | pubmed:articleTitle | Hippocampectomy disrupts trace eye-blink conditioning in rabbits. | lld:pubmed |
pubmed-article:2346619 | pubmed:affiliation | Department of Cell, Molecular, and Structural Biology, Northwestern University Medical School, Chicago, Illinois 60611. | lld:pubmed |
pubmed-article:2346619 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:2346619 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
pubmed-article:2346619 | pubmed:publicationType | Research Support, U.S. Gov't, Non-P.H.S. | lld:pubmed |
pubmed-article:2346619 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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