Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0751295 (memory loss)
 3,619 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Effects of the nimodipine, L-type calcium channel antagonist, has been studied on memory loss caused by spontaneous morphine withdrawal in mice. Mice were made dependent by increasing doses of morphine over three days. Memory was evaluated using object recognition task, which is based on tendency of rodents to exploration of new objects. The test was comprised of three sections: 15 min habitation, 12 min first trial and 5 min test trial. Recognition index was evaluated 4h after the last dose of morphine. Nimodipine was administrated either in chronic form (1, 5 and 10mg/kg) with daily doses of morphine or it was given as a single injection (5 and 10mg/kg) on the last day. Nimodipine in both treatment forms prevented the memory impairment following spontaneous morphine withdrawal. Corticosterone concentration was increased in brain and blood of mice during abstinence phase and pretreatment with nimodipine prevented the increase in brain and blood corticosterone concentration. The results show that blockade of L-type calcium channels improves memory deficits caused by morphine withdrawal. This indicates that some kind of treatments, such as nimodipine, administrated over the acute withdrawal phase, can prevent memory deficit during withdrawal.
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PMID:The effect of nimodipine on memory impairment during spontaneous morphine withdrawal in mice: Corticosterone interaction. 2298 64

Chronic exposure to hypobaric hypoxia (HH) causes neurodegeneration and loss of memory. The underlying mechanisms of HH induced memory impairment have been attributed to prolonged elevated corticosterone level in hippocampus leading to augmented glutamate excitotoxicity, oxidative stress, alteration of neurotransmitter level or their receptors and calcium mediated signaling. Whether this corticosterone mediated neurodegenerative effect occurs through overstimulation of glucocorticoid receptors (GRs) or is independent of the GRs, is not known. Four groups of rats were taken and GR blocker mifepristone was administered intraperitoneally during exposure to HH from 3rd to 7th days. Our results showed a duration dependent transcriptional upregulation of GRs and MRs following exposure to HH. Prolonged exposure to HH for 7 days augmented the translocation of GRs from cytosol to nucleus. Inhibition of GRs during hypoxic exposure improved the hippocampal ATP level and modulated the apoptotic markers like p53, Bcl(2) and Bax. Decreased expression of L-type calcium channel and NR1 subunit of NMDA receptors were also observed following administration of mifepristone during hypoxic exposure. Morphological studies following mifepristone administration during hypoxic exposure showed decreased number of pyknotic cells in hippocampus and decrease in apoptotic and necrotic cells in the CA3 region of hippocampus. The study indicates that elevated corticosterone level during hypoxic exposure causes neurodegeneration and acts through its binding to GRs indicating that inhibition of GRs may provide therapeutic effect in ameliorating HH induced memory impairment.
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PMID:Inhibition of glucocorticoid receptors ameliorates hypobaric hypoxia induced memory impairment in rat. 2315 6

We have previously evaluated the effect of nimodipine, L-type calcium channel blocker, on memory loss during spontaneous morphine withdrawal. In the present study the effect of nimodipine on memory loss in naloxone-induced morphine withdrawal mice was investigated. Mice were made dependent by increasing doses of morphine for three days. Object recognition task that was used for evaluation of memory performance comprised of three sections: 15 min habitation, 12 min first trial and 5 min test trial. Naloxone was injected 3 h after the administration of the last dose of morphine. Recognition index was evaluated 20 min after naloxone injection. Nimodipine was administrated in repeated form (1, 5 and 10 mg/kg) with daily doses of morphine or as a single injection (5 and 10 mg/kg) on the last day. Both acute and repeated treatments with nimodipine prevented the memory impairment in naloxone-induced morphine withdrawal mice (P<0.05 comparison of acute and repeated treatment data with their corresponding control values). Corticosterone concentration was significantly increased in the brain and blood of the mice during withdrawal. Pretreatment with nimodipine, however, decreased the corticosterone concentration in both brain and blood. The present study showed that nimodipine prevents intense memory loss following naloxone-induced morphine withdrawal.
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PMID:The effect of nimodipine on memory loss following naloxone-induced morphine withdrawal in object recognition. 2633 59