Neuroscience 2004 Abstract
| Presentation Number: | 379.8 |
|---|---|
| Abstract Title: | Detection of neural damage in the hippocampal CA1 using manganese-enhanced MRI (MEMRI) in a four-vessel occlusion model. |
| Authors: |
Mori, Y.*1
; Aoki, I.2
; Ebisu, T.3
; Umeda, M.2
; Higuchi, T.1
; Naruse, S.4
; Tanaka, C.1,2
1Dept. of Neurosurgery, Meiji Univ. of Oriental Med., Kyoto, Japan 2Dept. of Med. Informatics, Meiji Univ. of Oriental Med., Kyoto, Japan 3Japan, 1 Hinotani Hiyoshi-cho, 629-0392, 4Dept. of Neurosurgery, 1 Hinotani Hiyoshi-cho, 629-0392, |
| Primary Theme and Topics |
Neurological and Psychiatric Conditions - Ischemia -- Global Ischemia |
| Secondary Theme and Topics | Neurological and Psychiatric Conditions<br />- Ischemia<br />-- Excitotoxicity and cell death |
| Session: |
379. Global Ischemia II Slide |
| Presentation Time: | Monday, October 25, 2004 9:45 AM-10:00 AM |
| Location: | San Diego Convention Center - Room 30E |
| Keywords: | ISCHEMIA, MODEL, HIPPOCAMPUS, MRI |
Manganese chloride (MnCl2) can selectively enter the ventricles within a few minutes after systemic administration and enhanced MR signals of hippocampal formation in one day. Therefore, manganese enhancement could be a good indicator to detect ischemic cells in the hippocampus. The aim of this study was to determine whether manganese-enhanced MRI (MEMRI) can be used to visualize neuronal death in the hippocampus after transient global ischemia.
Nine male Wistar rats were divided into two groups; a sham-operated control group (n = 5) and a group subjected to ischemia (n = 4). An ischemia was induced using the four-vessel occlusion method described by Pulsinelli et al. The vertebral arteries were permanently occluded at the first cervical vertebra. On the following day, the animals subjected to ischemia were induced to a 10-minute transient global ischemia by clamping the carotid arteries. At 14 days after ischemia, the animals were infused with a 50 mM MnCl2 solution. Two days after the MnCl2 infusion, the animals were re-anesthetized to acquire MRI.
MRI measurements were performed in a 4.7-Tesla magnet and T1-weighted MRI were acquired using a conventional spin-echo sequence. After the MRI acquisitions, the brains were removed for histopathologic evaluation.
On MEMRI, signal enhancement was observed in the CA1 and CA3 regions of the sham-operated control group. In contrast, in the group that underwent ischemia, significant signal loss was selectively observed only in the CA1 at 14 days after occlusion, consistent with histologic findings such as pyknosis. This study suggests that MEMRI can be possibly used to evaluate the process of neuronal death in vulnerable regions such as the CA1.
Nine male Wistar rats were divided into two groups; a sham-operated control group (n = 5) and a group subjected to ischemia (n = 4). An ischemia was induced using the four-vessel occlusion method described by Pulsinelli et al. The vertebral arteries were permanently occluded at the first cervical vertebra. On the following day, the animals subjected to ischemia were induced to a 10-minute transient global ischemia by clamping the carotid arteries. At 14 days after ischemia, the animals were infused with a 50 mM MnCl2 solution. Two days after the MnCl2 infusion, the animals were re-anesthetized to acquire MRI.
MRI measurements were performed in a 4.7-Tesla magnet and T1-weighted MRI were acquired using a conventional spin-echo sequence. After the MRI acquisitions, the brains were removed for histopathologic evaluation.
On MEMRI, signal enhancement was observed in the CA1 and CA3 regions of the sham-operated control group. In contrast, in the group that underwent ischemia, significant signal loss was selectively observed only in the CA1 at 14 days after occlusion, consistent with histologic findings such as pyknosis. This study suggests that MEMRI can be possibly used to evaluate the process of neuronal death in vulnerable regions such as the CA1.
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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