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海人酸损伤的海马体是否会变得具有致痫性?

Do kainate-lesioned hippocampi become epileptogenic?

作者信息

Franck J E, Schwartzkroin P A

出版信息

Brain Res. 1985 Mar 11;329(1-2):309-13. doi: 10.1016/0006-8993(85)90540-2.

DOI:10.1016/0006-8993(85)90540-2
PMID:3978453
Abstract

Kainic acid lesions of hippocampal subfields CA3-CA4 produced dramatic synchronous afterdischarge activity in subfield CA1 when studied 2-4 weeks post-lesion in the in vitro slice preparation. This epileptiform discharge was correlated with a loss of intrinsic firing-induced afterhyperpolarizations and synaptic IPSPs. Two to 4 months post-lesion, intrinsic afterpotentials and synaptic inhibition appeared normal in most cells studied.

摘要

在体外脑片制备中,损伤后2 - 4周进行研究时,海马亚区CA3 - CA4的红藻氨酸损伤在CA1亚区产生了显著的同步后放电活动。这种癫痫样放电与内在放电诱导的超极化后电位和突触抑制性突触后电位的丧失有关。损伤后2至4个月,在大多数研究的细胞中,内在后电位和突触抑制似乎正常。

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1
Do kainate-lesioned hippocampi become epileptogenic?海人酸损伤的海马体是否会变得具有致痫性?
Brain Res. 1985 Mar 11;329(1-2):309-13. doi: 10.1016/0006-8993(85)90540-2.
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Neurosci Lett. 1981 Nov 18;27(1):31-6. doi: 10.1016/0304-3940(81)90201-9.

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Neocortical post-traumatic epileptogenesis is associated with loss of GABAergic neurons.新皮质创伤后癫痫发生与γ-氨基丁酸能神经元的丧失有关。
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Changes in hippocampal circuitry after pilocarpine-induced seizures as revealed by opioid receptor distribution and activation.通过阿片受体分布和激活揭示的毛果芸香碱诱发癫痫后海马回路的变化。
J Neurosci. 1997 Jan 1;17(1):477-92. doi: 10.1523/JNEUROSCI.17-01-00477.1997.
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