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THE NMDA ANTAGONIST, MD-801, SUPPRESSES LONG-TERM POTENTIATION, KINDLING, AND KINDLING-INDUCED POTENTIATION IN THE PERFORANT PATH OF THE UNANESTHETIZED RAT
Citation:
Gilbert, M. AND C. Mack. THE NMDA ANTAGONIST, MD-801, SUPPRESSES LONG-TERM POTENTIATION, KINDLING, AND KINDLING-INDUCED POTENTIATION IN THE PERFORANT PATH OF THE UNANESTHETIZED RAT. U.S. Environmental Protection Agency, Washington, D.C., EPA/600/J-90/170 (NTIS PB91116087), 1990.
Description:
Antagonism of NMDA-mediated transmission by MK-801 has been shown to block long-term potentiation (LTP) in vitro and delay electrical kindling of the amygdala. he present experiment sought to examine the relationship between synaptic potentiation of the perforant path-granule cell synapse and development of perforant path kindling. K-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. he 1.0 mg/kg dosage also increased after discharge (AD) thresholds, delayed kindling development from daily stimulation of the perforant path (c = 8.82 + and 22.9 + 3.66 sessions to the first stage 5 seizure), and increased AD durations. indling produced a significant potentiation of the EPSP (47%) and population spike (49%) after the first evoked AD in control animals. o significant enhancement of either component of the field potential was observed in MD-801-treated animals. nimals treated with this dosage of MD-801, did, however, kindle in the absence of potentiation at this synapse. t was concluded that although NMDA-mediated potentiation may facilitate kindling, synaptic potentiation does not appear to be a critical requirement for response and not synaptic enhancement may be the critical physiological alteration that underlies the kindling phenomenon.