LONG-TERM POTENTIATION IN HIPPOCAMPAL-CA1 - EFFECTS OF AFTERDISCHARGES, NMDA ANTAGONISTS, AND ANTICONVULSANTS

被引:35
作者
LEUNG, LS [1 ]
SHEN, B [1 ]
机构
[1] UNIV WESTERN ONTARIO,DEPT CLIN NEUROL SCI,LONDON N6A 5A5,ONTARIO,CANADA
关键词
D O I
10.1006/exnr.1993.1022
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Long-term potentiation (LTP) of the basal dendritic population excitatory postsynaptic potential (EPSP) in hippocampal CA1 was readily elicited in behaving rats, without afterdischarges (ADs), by θ-frequency-patterned primed bursts (PBs) delivered to the contralateral CA1. A long-lasting postictal potentiation (PIP) was also elicited by high-frequency trains (1 s at 200 Hz), following an AD and a 5- to 10-min depression. The N -methyl-d-aspartate (NMDA) antagonist 2-amino-phosphonovalerate was effective in blocking both LTP and PIP. The noncompetitive NMDA antagonist MK801 (0.5 mg/kg ip) attenuated the PB-induced LTP but enhanced PIP. The anticonvulsants phenytoin (40 mg/kg ip) and U54494A (25 or 50 mg/kg ip) had no effects on the LTP induced by a PB but they, like MK801, enhanced PIP to various degrees. The apparent enhancement of PIP by anticonvulsants may be a direct result of shortening the hippocampal AD duration and alleviation of the postictal EPSP depression. It is inferred that the typical hippocampal AD did not induce potentiation, but rather a postictal depression of the EPSP or a suppression of LTP. The mechanism of the postictal depression is likely different from the NMDA receptor-mediated LTP and PIP and it may depend on the AD duration (and perhaps excessive Ca2+ influx) but not critically on NMDA receptors. © 1993 Academic Press, Inc.
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页码:205 / 214
页数:10
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