Axon terminal hyperexcitability associated with epileptogenesis in vitro. II. Pharmacological regulation by NMDA and GABAA receptors.
Axon terminal hyperexcitability associated with epileptogenesis in vitro. II. Pharmacological regulation by NMDA and GABAA receptors.
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轴突末端过度兴奋与体外癫痫发生相关。
DOI：
10.1152/jn.1993.70.3.976
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发表时间：
1993
影响因子：
2.5
通讯作者：
Wilson,WA
中科院分区：
文献类型：
--
作者：
Stasheff,SF;Mott,DD;Wilson,WA
1.先前的报告提供的证据表明，点燃样诱导的电描记癫痫发作（EGS）在海马切片伴随着持续增加的兴奋性CA 3轴突终末，这是表现为增加在该网站的动作电位启动。在这份报告中，我们探讨了N-甲基-D-天冬氨酸（NMDA）受体在诱导和维持这种逆向放电中的作用，以及γ-氨基丁酸A型（GABAA）受体在调节这种活动中的作用，一旦它被诱导。2.点燃样刺激序列（60 Hz，2 s）被递送至s。每隔10分钟，对CA 3区放射状突起进行一次扫描。在对照人工脑脊液（ACSF）中，EGS的轴突终末放电频率显著增加（10.33 ± 3.29峰/分，平均± SE P < 0.01）。竞争性NMDA拮抗剂D-2-氨基-5-膦酰基戊酸（D-APV，50或100 μ M）的预先应用阻止了EGS的诱导，并抑制了在对照ACSF中观察到的终末放电的增加（平均增加1.06 +/-1.11峰/分钟，P < 0.02）。然而，当仅在对照ACSF中诱导EGS和逆向棘波后应用D-APV时，它不能改变终末放电频率（对照ACSF中平均6.44 ± 2.03，APV中平均8.89 ± 2.31; P >> 0.1）。因此，NMDA受体是诱导所需的，但不是维持轴突终末放电增加，因为我们以前已经证明是EGSs的情况。（250字处删节）
1. The preceding report presented evidence that the kindling-like induction of electrographic seizures (EGSs) in the hippocampal slice is accompanied by a lasting increase in the excitability of CA3 axon terminals, which is manifested by an increase in action-potential initiation at this site. In this report we explore the role of the N-methyl-D-aspartate (NMDA) receptor in the induction and maintenance of this antidromic firing, as well as the role of the gamma-aminobutyric acid type A (GABAA) receptor in regulating this activity once it has been induced. 2. Kindling-like stimulus trains (60 Hz, 2 s) were delivered to s. radiatum of CA3 at 10-min intervals. As EGSs developed in control artificial cerebrospinal fluid (ACSF), the frequency of axon terminal firing increased markedly (by 10.33 +/- 3.29 spikes/min, mean +/- SE P << 0.01). The prior application of the competitive NMDA antagonist D-2-amino-5-phosphonovaleric acid (D-APV, 50 or 100 microM) prevented the induction of EGSs and suppressed the increase in terminal firing seen in control ACSF (mean increase 1.06 +/- 1.11 spikes/min, P < 0.02). However, when D-APV was applied only after EGSs and antidromic spikes were induced in control ACSF, it failed to alter the frequency of terminal firing (mean 6.44 +/- 2.03 in control ACSF, 8.89 +/- 2.31 in APV; P >> 0.1). Thus the NMDA receptor is required for the induction but not maintenance of increased axon terminal firing, as we previously have shown to be the case for EGSs.(ABSTRACT TRUNCATED AT 250 WORDS)