This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map 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 Hatakeyama, T. Articles by Yanagihara, T. Search for Related Content PubMed PubMed Citation Articles by Hatakeyama, T. Articles by Yanagihara, T.

Stroke, Vol 19, 1526-1534, Copyright © 1988 by American Heart Association

ARTICLES

Immunohistochemical investigation of ischemic and postischemic damage after bilateral carotid occlusion in gerbils

T Hatakeyama, M Matsumoto, JM Brengman and T Yanagihara
Department of Neurology, Mayo Clinic, Rochester, MN 55905.

We investigated progression and recovery of neuronal damage during and after global cerebral ischemia in gerbils after bilateral occlusion of the common carotid arteries, using the immunohistochemical method (reaction for tubulin and creatine kinase BB-isoenzyme). The earliest, but reversible, ischemic lesions occurred after 3 minutes' ischemia in the subiculum-CA1 and CA2 regions of the hippocampus. The lesions became irreversible after 4 minutes' ischemia. The ischemic and postischemic lesions in the cerebral cortex, thalamus, and caudoputamen were partially or completely reversible if the ischemic period was 5 minutes, whereas delayed degeneration occurred in the pyramidal cells of the medial CA1 region after reperfusion for 48 hours (delayed neuronal death). After 10 minutes' ischemia and subsequent reperfusion, delayed neuronal death extended from the medial to the lateral CA1 region; the ischemic and postischemic lesions in the cerebral cortex, thalamus, and caudoputamen also expanded during reperfusion. Our investigation demonstrates that selective vulnerability existed in global cerebral ischemia as in incomplete or regional ischemia and suggests that neurons in many areas of the brain possessed the potential for recovery, progressive deterioration, and even delayed neuronal death depending on the severity and duration of cerebral ischemia.

This article has been cited by other articles:

				K. R. Dave, R. A. DeFazio, A. P. Raval, A. Torraco, I. Saul, A. Barrientos, and M. A. Perez-Pinzon Ischemic Preconditioning Targets the Respiration of Synaptic Mitochondria via Protein Kinase C{varepsilon} J. Neurosci., April 16, 2008; 28(16): 4172 - 4182. [Abstract] [Full Text] [PDF]

				C. Sommer and M. Kiessling Ischemia and Ischemic Tolerance Induction Differentially Regulate Protein Expression of GluR1, GluR2, and AMPA Receptor Binding Protein in the Gerbil Hippocampus: GluR2 (GluR-B) Reduction Does Not Predict Neuronal Death Stroke, April 1, 2002; 33(4): 1093 - 1100. [Abstract] [Full Text] [PDF]

				J. A. Connor and R. J. Cormier Cumulative Effects of Glutamate Microstimulation on Ca2+ Responses of CA1 Hippocampal Pyramidal Neurons in Slice J Neurophysiol, January 1, 2000; 83(1): 90 - 98. [Abstract] [Full Text] [PDF]

				W. I. Rosenblum, K. Kitagawa, M. Matsumoto, and M. R. Pulera Apoptosis and Stroke Pathogenesis • Response • Response Stroke, May 1, 1999; 30(5): 1154 - 1156. [Full Text] [PDF]

				A. Shiino, M. Matsuda, J. Handa, B. Chance, and H. A. Kontos Poor Recovery of Mitochondrial Redox State in CA1 After Transient Forebrain Ischemia in Gerbils • Editorial Comment Stroke, November 1, 1998; 29(11): 2421 - 2425. [Abstract] [Full Text] [PDF]

				J.-Y. Li, H. Ueda, A. Seiyama, M. Nakano, M. Matsumoto, and T. Yanagihara A Near-Infrared Spectroscopic Study of Cerebral Ischemia and Ischemic Tolerance in Gerbils Stroke, July 1, 1997; 28(7): 1451 - 1457. [Abstract] [Full Text]

				O. Takemoto, H. Tomimoto, and T. Yanagihara Induction of c-fos and c-jun Gene Products and Heat Shock Protein After Brief and Prolonged Cerebral Ischemia in Gerbils Stroke, September 1, 1995; 26(9): 1639 - 1648. [Abstract] [Full Text]

				K. Abe, M. Aoki, J. Kawagoe, T. Yoshida, A. Hattori, K. Kogure, and Y. Itoyama Ischemic Delayed Neuronal Death : A Mitochondrial Hypothesis Stroke, August 1, 1995; 26(8): 1478 - 1489. [Abstract] [Full Text]