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海人藻酸/使君子氨酸受体拮抗剂CNQX可阻断大鼠海马器官型培养物中自发性癫痫样活动的快速成分。

The kainate/quisqualate receptor antagonist, CNQX, blocks the fast component of spontaneous epileptiform activity in organotypic cultures of rat hippocampus.

作者信息

McBain C J, Boden P, Hill R G

机构信息

Parke-Davis Research Unit, Cambridge, U.K.

出版信息

Neurosci Lett. 1988 Nov 11;93(2-3):341-5. doi: 10.1016/0304-3940(88)90106-1.

DOI:10.1016/0304-3940(88)90106-1
PMID:2907375
Abstract

Intracellular recordings were made from CA1 pyramidal neurones of hippocampus maintained in organotypic culture. Both spontaneous interictal and ictal epileptiform activity was observed. CNQX, an antagonist at kainate/quisqualate but not at N-methyl-D-aspartate (NMDA)-sensitive excitatory amino acid receptors depressed but did not abolish spontaneous epileptiform activity. Addition of the specific NMDA receptor antagonist D-2-amino-5-phosphonovalerate (D-APV) abolished the remaining activity. Similar effects were observed on electrically evoked excitatory post synaptic potentials (EPSPs). This suggests a role for endogenous excitatory amino acids acting at both kainate/quisqualate and NMDA sensitive excitatory amino acid receptors in the generation and maintainance of epileptiform activity within these organotypic cultures.

摘要

对维持在器官型培养中的海马CA1锥体神经元进行细胞内记录。观察到了自发性发作间期和发作期癫痫样活动。CNQX是一种对海人藻酸/quisqualate敏感但对N-甲基-D-天冬氨酸(NMDA)敏感的兴奋性氨基酸受体无拮抗作用的拮抗剂,它可抑制但不能消除自发性癫痫样活动。加入特异性NMDA受体拮抗剂D-2-氨基-5-磷酸戊酸(D-APV)可消除剩余活动。在电诱发的兴奋性突触后电位(EPSP)上也观察到了类似的效应。这表明内源性兴奋性氨基酸在这些器官型培养物中癫痫样活动的产生和维持过程中,对海人藻酸/quisqualate敏感和NMDA敏感的兴奋性氨基酸受体均起作用。

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