This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Seren, M. S. Articles by Leon, A. Search for Related Content PubMed PubMed Citation Articles by Seren, M. S. Articles by Leon, A. Pubmed/NCBI databases Compound via MeSH Substance via MeSH Medline Plus Health Information Transient Ischemic Attack

Stroke, Vol 21, 1607-1612, Copyright © 1990 by American Heart Association

ARTICLES

Protective effects of a monosialoganglioside derivative following transitory forebrain ischemia in rats

MS Seren, R Rubini, A Lazzaro, R Zanoni, MG Fiori and A Leon
Fidia Research Laboratories, Abano Terme, Italy.

We evaluated the effects of treatment with the inner ester derivative of the monosialoganglioside GM1 on cortical electroencephalographic activity and hippocampal CA1 morphology after transitory, near-complete cerebral ischemia in rats. Ischemia was induced by the four-vessel occlusion method, and we studied only the 58 rats that showed flattening of the cortical electroencephalogram for the entire 30 minutes of occlusion. The ganglioside (n = 30) or saline (n = 28) was administered intravenously immediately after release of the carotid clips and then intramuscularly for 21 days of observation. Cortical electroencephalographic activity was monitored throughout the experiment. After 21 days of recirculation we assessed hippocampal CA1 damage by light microscopy. The results indicate that treatment with the ganglioside reduces postischemic secondary damage to the cortical circuitry (as indicated by significantly higher cortical electroencephalographic activity late after reperfusion) and limits neuronal loss in the CA1 region. Our results lend support to the possible therapeutic use of ganglioside in human pathologic conditions associated with cerebrovascular insufficiencies.

This article has been cited by other articles:

				S. J. Rabin, A. Bachis, and I. Mocchetti Gangliosides Activate Trk Receptors by Inducing the Release of Neurotrophins J. Biol. Chem., December 13, 2002; 277(51): 49466 - 49472. [Abstract] [Full Text] [PDF]

				B. R. Ryu, D. W. Choi, D. M. Hartley, E. Costa, I. Jou, and B. J. Gwag Attenuation of Cortical Neuronal Apoptosis by Gangliosides J. Pharmacol. Exp. Ther., August 1, 1999; 290(2): 811 - 816. [Abstract] [Full Text]

				G. Ferrari, B. L. Anderson, R. M. Stephens, D. R. Kaplan, and L. A. Greene Prevention of Apoptotic Neuronal Death by G[IMAGE] Ganglioside J. Biol. Chem., February 17, 1995; 270(7): 3074 - 3080. [Abstract] [Full Text] [PDF]