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The Journal of Neurophysiology Vol. 82 No. 2 August 1999, pp. 736-740
Copyright ©1999 by the American Physiological Society
Northeastern Ohio Universities College of Medicine, Department of Neurobiology, Rootstown, Ohio 44272-0095
Morgan, S. L. and
T. J. Teyler.
VDCCs and NMDARs Underlie Two Forms of LTP in CA1 Hippocampus In
Vivo. J. Neurophysiol. 82: 736-740, 1999. N-methyl-D-aspartate
receptor/channel (NMDAR) and voltage-dependent calcium channel (VDCC)
antagonists applied independently reduce the magnitude of long-term
potentiation (LTP) in area CA1 of the hippocampal slice preparation.
When used in combination, the antagonists completely block the
induction of LTP. In urethan-anesthetized rats we examined the effect
of the NMDAR blocker MK-801 (0.1 mg/kg) and the VDCC blocker Verapamil
(10 mg/kg) on LTP induction in area CA1. Extracellular recordings were
obtained from stratum radiatum following stimulation of Schaffer
collaterals. LTP was induced by a 200-Hz/100-ms tetanus repeated 10 times (2 s isi). Tetanus was given in the presence of intraperitoneal
saline, MK-801, Verapamil, or both Verapamil and MK-801. When given
separately, Verapamil and MK-801 both significantly reduced the
magnitude of LTP as compared with control animals. When given together, the drugs blocked the induction of LTP completely. We conclude that
like LTP in vitro, VDCCs and NMDAR underlie two forms of LTP in vivo.
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