rdf:type |
|
lifeskim:mentions |
|
pubmed:issue |
2
|
pubmed:dateCreated |
1990-7-20
|
pubmed:abstractText |
The nicotinic antagonist mecamylamine (2.5 and 5 mg/kg/IP) depressed both active (shuttle-box) and passive (step-through) avoidance learning in mice of the DBA/2 strain. The nootropic drug oxiracetam (50 and 100 mg/kg/IP) improved acquisition in the multitrial active avoidance test, but had no effect on one-trial passive avoidance learning. When the two drugs were combined, oxiracetam did not counteract mecamylamine-induced impairment of passive avoidance learning, even if it maintained a facilitating action on shuttle-box avoidance acquisition in mice receiving the nicotinic receptor blocker. Prevention of mecamylamine-induced shuttle-box avoidance depression by oxiracetam indicates that central nicotinic mechanisms are probably involved in the improving effects exerted by nootropic drugs on learning.
|
pubmed:language |
eng
|
pubmed:journal |
|
pubmed:citationSubset |
IM
|
pubmed:chemical |
|
pubmed:status |
MEDLINE
|
pubmed:month |
Jun
|
pubmed:issn |
0091-3057
|
pubmed:author |
|
pubmed:issnType |
Print
|
pubmed:volume |
36
|
pubmed:owner |
NLM
|
pubmed:authorsComplete |
Y
|
pubmed:pagination |
389-92
|
pubmed:dateRevised |
2003-11-14
|
pubmed:meshHeading |
pubmed-meshheading:2356212-Animals,
pubmed-meshheading:2356212-Avoidance Learning,
pubmed-meshheading:2356212-Drug Interactions,
pubmed-meshheading:2356212-Electric Stimulation,
pubmed-meshheading:2356212-Male,
pubmed-meshheading:2356212-Mecamylamine,
pubmed-meshheading:2356212-Mice,
pubmed-meshheading:2356212-Mice, Inbred DBA,
pubmed-meshheading:2356212-Motor Activity,
pubmed-meshheading:2356212-Nicotinic Antagonists,
pubmed-meshheading:2356212-Pain,
pubmed-meshheading:2356212-Psychotropic Drugs,
pubmed-meshheading:2356212-Pyrrolidines,
pubmed-meshheading:2356212-Sensory Thresholds
|
pubmed:year |
1990
|
pubmed:articleTitle |
Oxiracetam prevents mecamylamine-induced impairment of active, but not passive, avoidance learning in mice.
|
pubmed:affiliation |
Istituto di Psicobiologia e Psicofarmacologia, CNR, Roma, Italy.
|
pubmed:publicationType |
Journal Article
|