SPROUTING OF GABAERGIC AND MOSSY FIBER AXONS IN DENTATE GYRUS FOLLOWING INTRAHIPPOCAMPAL KAINATE IN THE RAT
SPROUTING OF GABAERGIC AND MOSSY FIBER AXONS IN DENTATE GYRUS FOLLOWING INTRAHIPPOCAMPAL KAINATE IN THE RAT
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DOI：
10.1016/0014-4886(90)90072-z
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发表时间：
1990-08-01
影响因子：
5.3
通讯作者：
BABB, TL
中科院分区：
文献类型：
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作者：
DAVENPORT, CJ;BROWN, WJ;BABB, TL
本研究检查了假定的γ-氨基丁酸（GABA能）抑制轴突和苔藓纤维（假定兴奋性）复发性侧支后，海马内注射赖氨酸（KA）。谷氨酸脱羧酶免疫反应性（GAD-IR）用于研究在单侧注射0.5 μ g KA/0.2 μ l到大鼠（n = 16）的后海马中后抑制轴突末端发芽，存活期为14、28和120天。年龄匹配的对照动物（n = 9）接受海马内0.2 μ l盐水（假手术，n = 4）或不注射（正常，n = 5）。为了研究苔藓纤维突触重排，将0.5 μ g KA/0.2 μ l体积单侧注射到大鼠（n = 10）的后海马中，存活期为14、28和120天，并将Timm硫化物染色的组织切片与年龄匹配的假手术组（n = 4）或正常对照组（n = 4）进行比较。在后KA注射后14至120天，与假手术或正常对照组相比，在同侧和对侧齿状筋膜（FD）的内分子层（IML）中GAD-IR斑点显著增加。KA损伤还诱导苔藓纤维复发侧支出芽进入同侧和对侧FD IMLs。的连合和同侧的关联传入的FD的损失显然诱导发芽到同侧和对侧终止区的颗粒细胞苔藓纤维和GAD-IR轴突，从而建立和异常电路附近观察到的病理红藻氨酸癫痫模型。虽然苔藓纤维产生单突触兴奋的反应性突触发生可能是KA致痫性的一种机制，但在FD的同一IML区中同时出现GABA能末梢表明异常抑制性突触可能导致慢性KA海马过度兴奋。
The present study examined the bilateral synaptic rearrangements of presumed .gamma.-aminobutyric acid (GABAergic) inhibitory axons and mossy fiber (presumed excitatory) recurrent collaterals following intrahippocampal lainic acid (KA) injection. Glutamate decarboxylase immunoreactivity (GAD-IR) was used to study inhibitory axon terminal sprouting, following 0.5 .mu.g KA/0.2 .mu.l injected unilaterally into the posterior hippocampus of rats (n = 16), with survival periods of 14, 28, and 120 days. The age-matched control animals (n = 9) received intrahippocampal 0.2 .mu.l saline (sham, n = 4) or no injection (normal, n = 5). To study mossy fiber synaptic rearrangements, 0.5 .mu.g KA/0.2 .mu.l volumes were injected unilaterally into the posterior hippocampus of rats (n = 10), with survival periods from 14, 28, and 120 days, and Timm sulfide-stained tissue sections were compared to age-matched sham (n = 4) or normal controls (n = 4). At 14 through 120 days after posterior KA injection, GAD-IR puncta were significantly increased in the ipsi- and contralateral inner molecular layers (IML) of the fascia dentata (FD) when compared to sham or normal controls. KA lesion also induced mossy fiber recurrent collateral sprouting into the ipsi and contralateral FD IMLs. The loss of both the commissural and ipsilateral associational afferents to the FD apparently induced sprouting into their ipsi- and contralateral termination zones by granule cell mossy fibers and GAD-IR axons, thus establishing and abnormal circuitry near the observed pathology in the kainate model of epilepsy. Although reactive synaptogenesis of mossy fibers producing monosynaptic excitation may be one mechanism for KA epileptogenicity, the concurrent sprouting of GABAergic terminals in the same IML zone of the FD suggests that anomalous inhibitory synapses may contribute to chronic KA hippocampal hyperexcitability.