Lee W L, Hablitz J J
Neurobiology Research Center, University of Alabama, Birmingham 35294.
Epilepsy Res. 1990 Jul;6(2):87-94. doi: 10.1016/0920-1211(90)90082-7.
Intracellular recordings were obtained from hippocampal CA1 and CA3 pyramidal neurons maintained in vitro. The ability of the NMDA receptor antagonists ketamine and APV to suppress picrotoxin-induced epileptiform burst activity was examined. Activity was recorded either after a single orthodromic stimulation, which gave rise to paroxysmal depolarization shift (PDS), or during a 500 msec train of 50 Hz stimulation, which produced a sustained depolarization. In the CA1 and CA3 areas, both the PDS and sustained depolarization were reduced by APV (20 microM) and ketamine (100 microM). APV reduced the area under the PDS by 24 +/- 3% and 32 +/- 4% in CA1 and CA3 neurons, respectively. The corresponding reductions in the sustained depolarization were 10 +/- 2% and 22 +/- 4%. Ketamine reduced the PDS by 43 +/- 4% and 31 +/- 4% in CA1 and CA3 and decreased the sustained depolarization by 21 +/- 3% and 12 +/- 3%. In all cases, NMDA receptor antagonists had a significantly greater effect on the PDS than the sustained depolarization. These results indicate that, although not essential for generation of paroxysmal activity, NMDA receptors make significant contributions to epileptiform activity in both CA1 and CA3 regions of the hippocampus.
从体外培养的海马CA1和CA3锥体神经元获得细胞内记录。研究了NMDA受体拮抗剂氯胺酮和APV抑制印防己毒素诱导的癫痫样爆发活动的能力。在单次顺向刺激后记录活动，该刺激会引起阵发性去极化偏移（PDS），或者在50 Hz刺激的500毫秒串刺激期间记录活动，该刺激会产生持续去极化。在CA1和CA3区域，APV（20 microM）和氯胺酮（100 microM）均降低了PDS和持续去极化。APV分别使CA1和CA3神经元中PDS下的面积减少了24±3%和32±4%。持续去极化的相应减少分别为10±2%和22±4%。氯胺酮使CA1和CA3中的PDS分别降低了43±4%和31±4%，并使持续去极化降低了21±3%和12±3%。在所有情况下，NMDA受体拮抗剂对PDS的影响均明显大于对持续去极化的影响。这些结果表明，尽管NMDA受体对于阵发性活动的产生并非必不可少，但它们对海马CA1和CA3区域的癫痫样活动有显著贡献。
