Neuroscience 2004 Abstract
Presentation Number: | 227.16 |
---|---|
Abstract Title: | Longitudinal study of hippocampal damage in kainic acid-induced limbic seizure in rat by high resolution diffusion-weighted, T2-weighted and manganese-enhanced magnetic resonance imaging. |
Authors: |
Hsu, Y.*1
; Tsai, W.1
; Chang, C.1
1Functional & Mircro-MRI Ctr, Inst Biomed Sci, Taipei, Taiwan Republic of China |
Primary Theme and Topics |
Neurological and Psychiatric Conditions - Epilepsy -- Human studies and animal models |
Session: |
227. Epilepsy: Basic Mechanisms I Poster |
Presentation Time: | Sunday, October 24, 2004 11:00 AM-12:00 PM |
Location: | San Diego Convention Center - Hall A-H, Board # YY16 |
Keywords: | EPILEPSY, MRI, NEURODEGENERATION |
The injection of kainic acid (KA) into rat elicits brain damages, including hippocampus, which mimic human temporal lobe epilepsy. Electrophysiological studies evidenced that KA induces epileptiform seizures first in hippocampal CA3 within 1 hr and then propagates to CA1 and other limbic structures. To gain further understanding of the hippocampal activation underlying KA-induced seizures, the aims of the present study are (1) to employ high resolution diffusion-weighted imaging (DWI) and T2-weighted imaging (T2WI) at high magnetic field (7 Tesla) to investigate the temporal evolution of hippocampal abnormalities induced by KA and (2) to investigate whether KA-induced CA3 neuronal activity can be detected using manganese (Mn2+)-enhanced MRI. DWI, T2WI and T1-weighted imaging (T1WI) were acquired before and 2 hr, 1 day¡V7 days after KA intravenous injection. The results showed that, in the dendrites of CA3 pyramidal cells, the hyperintensities of DWI and T2WI were both observed within 2 hr, indicating the formation of edema. Interestingly, in the soma of CA3 pyramidal cells, the signal intensity of T2WI was increased within 2 hr, whereas the signal intensity of DWI was decreased, suggesting neuronal degeneration. With Mn2+-enhanced MRI, the hyperintense region was only presented in the soma of CA3 pyramidal cells, suggesting Mn2+ accumulation may be located in KA-activated neurons not in edema, since Mn2+ enters neurons through opened voltage-gated Ca2+ channels during activation. The abnormal MR signal intensities in hippocampus declined 5 days post KA, reflecting gliosis. The present study demonstrates that high resolution MRI can detect KA-induced early subtle damages in hippocampus and Mn2+-enhanced MRI may be an invaluable tool to map neuronal activation directly in vivo.
Supported by a grant from National Science Council, Taiwan R.O.C.
Sample Citation:
[Authors]. [Abstract Title]. Program No. XXX.XX. 2004 Neuroscience Meeting Planner. San Diego, CA: Society for Neuroscience, 2004. Online.
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