Exp Neurobiol 2004; 13(2): 97-104
Published online December 31, 2004
© The Korean Society for Brain and Neural Sciences
Young-Sil Kim1, In-Koo Hwang2, Ki-Yeon Yoo2, Moo-Ho Won2 and Hyung-Cheul Shin1CA*
Departments of 1Physiology and 2Anatomy, College of Medicine,Hallym University, Chuncheon 200-702, Korea
Correspondence to: *To whom correspondence should be addressed.
TEL: +82-33-248-2585, FAX: +82-33-255-1640
Consequences of transient ischemia on the neuronal activity of hippocampal CA1 region were investigated in Mongolian gerbil. Ischemia was done for 5 min in two groups, such that in Group 1 it was done 1 week after implantation of recording micro-wire electrodes and in Group 2 immediately before electrode implantation. Pyramidal neurons of CA1 of anesthetized gerbils showed stable spontaneous activities before ischemia (5.21±0.54 Hz). Immediately after the initiation of ischemia, neurons in both groups showed initial cessation of spontaneous activity. Spike discharge reappeared about 5 min after recirculation. However neural activity was suppressed for 25 min of post- ischemia period. In both Group 1 and Group 2, some neurons (Type 1) showed full recovery of spontaneous activity by 6 h after ischemia and subsequent hyperactivity, but other neurons (Type 2) exhibited only partial recovery and subsequent deterioration of activity. Neural activity of Type 1 was maximally enhanced at post-ischemic 12 h & day 1 (Group 1: 97.31% and Group 2: 110.34%). Thereafter, CA1 activity was gradually de-creased to below the pre-ischemia level (-29.17% at day 3 in Group 1 and -44.95% at day 4 in Group 2). Histological analysis indicated that in both hemispheres CA1 cell death was observed in Group 2 but it was noticed only at small region in Group 1. Animals with implantation surgery but without ischemia did not show any cell death. The results of this study suggest that functional loss of CA1 activity and morphological death following ischemia in chronically implanted Mongolian gerbil could not occur in parallel.
Keywords: Transient ischemia, hippocampal CA1 pyramidal cells, temporal activity change