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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
2
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pubmed:dateCreated |
1997-6-12
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pubmed:abstractText |
The effects of N-methyl-D-aspartate receptor blockade on two major variants of rabbit eyeblink conditioning were evaluated using a selective noncompetitive antagonist, [5R, 10S]-[+]-5-methyl-10, 11-dihydro-5H-dibenzo[a, d] cyclo-hepten-5,10-imine hydrogen maleate; dizocilpine (MK-801) or phencyclidine (PCP), a drug of abuse. Either MK-801 or PCP (given daily) impaired rabbits' ability to associate tone conditioned stimuli with airpuff unconditioned stimuli, with the severity of impairment exhibiting clear dose and task dependencies. Trace-conditioned rabbits given > or = 80 micrograms/kg of MK-801 or > or = 1.0 mg/kg of PCP failed to reach a criterion of 80% conditioned responses during training, with significant impairments seen at intermediate doses. Delay-conditioned rabbits, although dose-dependently slowed, successfully acquired the task, even when given doses of MK-801 or PCP that completely blocked acquisition in trace conditioning. Additionally, even low doses of MK-801 (10 micrograms/kg) or of PCP (0.1 mg/kg) severely altered conditioned response timing in trace but not in delay conditioning, resembling effects observed after hippocampal lesions. Doses of MK-801 or PCP that impaired acquisition also severely impaired extinction of both trace- and delay-conditioned eyeblink responses. However, neither MK-801 nor PCP altered retention or timing of previously learned responses. Higher doses of MK-801 (> or = 200 micrograms/kg) or of PCP (> or = 2.0 mg/kg) dose-dependently impaired unconditioned response performance, although lower doses of MK-801 (< or = 160 micrograms/kg) or of PCP (< or = 1.0 mg/kg) had no effects on unconditioned responses or on non-associative pseudoconditioned responses. The deficits observed indicate that although not necessary for retention, N-methyl-D-aspartate receptor activation may facilitate acquisition of delay-conditioning. N-methyl-D-aspartate receptor activation appears to be necessary for acquisition of trace conditioning, and for extinction in either paradigm.
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Dizocilpine Maleate,
http://linkedlifedata.com/resource/pubmed/chemical/Excitatory Amino Acid Antagonists,
http://linkedlifedata.com/resource/pubmed/chemical/Phencyclidine,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, N-Methyl-D-Aspartate
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pubmed:status |
MEDLINE
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pubmed:month |
May
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pubmed:issn |
0022-3565
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
281
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
928-40
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pubmed:dateRevised |
2007-11-14
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pubmed:meshHeading |
pubmed-meshheading:9152403-Animals,
pubmed-meshheading:9152403-Conditioning, Eyelid,
pubmed-meshheading:9152403-Dizocilpine Maleate,
pubmed-meshheading:9152403-Dose-Response Relationship, Drug,
pubmed-meshheading:9152403-Excitatory Amino Acid Antagonists,
pubmed-meshheading:9152403-Female,
pubmed-meshheading:9152403-Phencyclidine,
pubmed-meshheading:9152403-Rabbits,
pubmed-meshheading:9152403-Receptors, N-Methyl-D-Aspartate
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pubmed:year |
1997
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pubmed:articleTitle |
N-methyl-D-aspartate receptors in associative eyeblink conditioning: both MK-801 and phencyclidine produce task- and dose-dependent impairments.
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pubmed:affiliation |
Department of Cell and Molecular Biology, Northwestern University Medical School, Chicago, Illinois, USA.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.
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