THE NMDA ANTAGONIST, MK-801, SUPPRESSES LONG-TERM POTENTIATION, KINDLING, AND KINDLING-INDUCED POTENTIATION IN THE PERFORANT PATH OF THE UNANESTHETIZED RAT
THE NMDA ANTAGONIST, MK-801, SUPPRESSES LONG-TERM POTENTIATION, KINDLING, AND KINDLING-INDUCED POTENTIATION IN THE PERFORANT PATH OF THE UNANESTHETIZED RAT
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DOI：
10.1016/0006-8993(90)90064-i
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发表时间：
1990-06-11
期刊：
影响因子：
2.9
通讯作者：
MACK, CM
中科院分区：
文献类型：
--
作者：
GILBERT, ME;MACK, CM
MK-801对NMDA介导的传递的拮抗作用已被证明可在体外阻断长时程增强（LTPP）并延迟杏仁核的电点燃。本实验旨在研究穿通通路-颗粒细胞突触的突触增强与穿通通路点燃发展之间的关系。MK-801（0.1和1.0 mg/kg）阻断了未麻醉动物在列车交付后24小时测量的穿支通路LTP的诱导。1.0 mg/kg剂量还增加了后放电（AD）阈值，延迟了由穿通通路的每日刺激引起的点燃发展（hivin x = 8.82 ± 0.01）。1.19和22.9 .+-。3.66第一阶段5发作），并增加AD持续时间。点燃产生了显着增强的EPSP（47%）和人口尖峰（49%）后，第一次诱发AD在对照组动物。在MK-801给药动物中未观察到场电位的任一分量显著增强。然而，接受该剂量MK-801治疗的动物在该突触缺乏增强作用的情况下确实点燃。得出的结论是，虽然NMDA介导的增强可能有助于点燃，突触增强似乎并不是点燃发展的关键要求。这些发现支持了这样一种观点，即爆发反应的发展而不是突触增强可能是点燃现象背后的关键生理变化。
Antagonism of NMDA-mediated transmission by MK-801 has been shown to block long-term potentiation (LTPP) in vitro and delay electrical kindling of the amygdala. The present experiment sought to examine the relationship between synaptic potentiation of the perforant path-granule cell synapse and development of perforant path kindling. MK-801 (0.1 and 1.0 mg/kg) blocked induction of LTP of the perforant path in the unanesthetized animal measured 24 h after train delivery. The 1.0 mg/kg dosage also increased afterdischarge (AD) thresholds, delayed kindling development from daily stimulation of the perforant path (.hivin.x = 8.82 .+-. 1.19 and 22.9 .+-. 3.66 sessions to the first stage 5 seizure), and increased AD durations. Kindling produced a significant potentiation of the EPSP (47%) and population spike (49%) after the first evoked AD in control animals. No significant enhancement of either component of the field potential was observed in MK-801-treated animals. Animals treated with this dosage of MK-801, did, however, kindle in the absence of potentiation at this synapse. It was concluded that although NMDA-mediated potentiation may facilitate kindling, synaptic potentiation does not appear to be a critical requirement for kindling to develop. These findings support the notion that development of the burst response and not synaptic enhancement may be the critical physiological alteration that underlies the kindling phenomenon.