Linked Life Data

14557723

Source:http://linkedlifedata.com/resource/pubmed/id/14557723

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
7
pubmed:dateCreated
2003-10-14
pubmed:abstractText
Cocaine (COC) has been reported to cause effects similar to physiological stressors in the brain neuroendocrinal system, including heat-shock protein (HSP) expression, although these effects have not been elucidated in detail. In the present study, we examined the effects of repeated (4 days) treatments with cocaine hydrochloride (35 mg/kg, i.p.) and 10 min immobilization stress (IM) on the distribution of HSP (HSP27, HSP60, HSP70, HSC70) and stress-activated protein kinase (SAPK) (SAPKalpha, SAPKbeta, SAPKgamma) immunoreactive nerve cells (positive cells) in the rat hippocampus. The swimming behaviors of the rats in the forced swimming test were also examined. In both COC and IM groups, an early enhancement (5 h time point) of hippocampal HSP (HSP27, HSP60, HSP70, HSC70) and SAPK (SAPKbeta, SAPKgamma) positive cells was observed, whereas a recovery (SAPKs) or attenuation (HSP60 and HSC70) was observed at the 24 h time point. In both groups, a depression of the swimming behaviors (attenuation in the activity counts and time until immobility) below the control level was observed at the 5 h point, but a recovery was observed at the 24 h time point. At the 48 h time point, all parameters returned to the control level. These alterations in the levels of HSPs and SAPKs, and the swimming behaviors were similar to those observed in the stress (IM) group, and were characteristic in that all of these alterations were attenuated by the benzodiazepine inverse agonist, Ro 15-4513 (5 mg/kg, i.p.), and the dopamine D1 receptor antagonist, SCH23390 (0.5 mg/kg, i.p.), which was not observed in the groups treated with another stressor-like drug (bicuculline).
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Nov
pubmed:issn
0955-8810
pubmed:author
pubmed:issnType
Print
pubmed:volume
14
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
551-62
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed-meshheading:14557723-Animals, pubmed-meshheading:14557723-Arousal, pubmed-meshheading:14557723-Azides, pubmed-meshheading:14557723-Benzazepines, pubmed-meshheading:14557723-Benzodiazepines, pubmed-meshheading:14557723-Cocaine, pubmed-meshheading:14557723-Dopamine Agonists, pubmed-meshheading:14557723-Escape Reaction, pubmed-meshheading:14557723-Heat-Shock Proteins, pubmed-meshheading:14557723-Hippocampus, pubmed-meshheading:14557723-Immobilization, pubmed-meshheading:14557723-Injections, Intraperitoneal, pubmed-meshheading:14557723-Male, pubmed-meshheading:14557723-Mitogen-Activated Protein Kinases, pubmed-meshheading:14557723-Motor Activity, pubmed-meshheading:14557723-Neurons, pubmed-meshheading:14557723-Rats, pubmed-meshheading:14557723-Rats, Wistar, pubmed-meshheading:14557723-Receptors, Dopamine D1, pubmed-meshheading:14557723-Stress, Psychological
pubmed:year
2003
pubmed:articleTitle
Similar effects of cocaine and immobilization stress on the levels of heat-shock proteins and stress-activated protein kinases in the rat hippocampus, and on swimming behaviors: the contribution of dopamine and benzodiazepine receptors.
pubmed:affiliation
Department of Legal Medicine, Kyoto University Graduate School of Medicine, Faculty of Medicine, Yoshidakanoe-cho, Sakyo-ku, Kyoto 606-8501, Japan. thayase@mri.biglobe.ne.jp
pubmed:publicationType
Journal Article