Protective Actions of Ghrelin on Global Cerebral Ischemia-Induced Memory Deficits

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Basaranlar G., DERİN N., Tan R., TANRIÖVER G., DEMİR N.

Neurophysiology, vol.46, no.4, pp.343-351, 2014 (SCI-Expanded) identifier identifier

  • Publication Type: Article / Article
  • Volume: 46 Issue: 4
  • Publication Date: 2014
  • Doi Number: 10.1007/s11062-014-9454-1
  • Journal Name: Neurophysiology
  • Journal Indexes: Science Citation Index Expanded (SCI-EXPANDED), Scopus
  • Page Numbers: pp.343-351
  • Keywords: transient global cerebral ischemia, ghrelin, hippocampus, caspase-3, total oxidant status, nitric oxide, NITRIC-OXIDE SYNTHASE, TRANSIENT FOREBRAIN ISCHEMIA, HIPPOCAMPAL DAMAGE, OXIDATIVE STRESS, RAT HIPPOCAMPUS, BRAIN ISCHEMIA, APOPTOSIS, INJURY, MODEL, EXPRESSION
  • Lokman Hekim University Affiliated: No


© 2014, Springer Science+Business Media New York.In our study, we investigated transient global cerebral ischemia (TGCI)-induced changes in spatial memory and motor activity together with apoptotic, oxidant, and NO/NOS signaling parameters in rats and the effects of treatment of animals with ghrelin. The TGCI-induced deficiencies of spatial memory and motor activity in the Y-maze and open field tests were attenuated by ghrelin treatment. Furthermore, ghrelin administration lowered the levels of caspase-3 and iNOS elevated by TGCI in the hippocampus. Thus, we conclude that ghrelin exerts a neuroprotective action against hippocampal TGCI injury via influencing apoptotic, oxidant, and/or NO/NOS pathways. If the underlying mechanisms of action of this agent are fully clarified, ghrelin might be a candidate drug for treatment of TGCI-induced memory impairments.