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N‐methyl‐D‐aspartate receptor antagonists are less effective in blocking long‐term potentiation at apical than basal dendrites in hippocampal CA1 of awake rats

N‐methyl‐D‐aspartate receptor antagonists are less effective in blocking long‐term potentiation... Long‐term potentiation (LTP) of field excitatory postsynaptic potentials (fEPSPs) at the apical or basal dendrites of CA1 pyramidal cells was induced by stimulation with a 1‐s train of 200‐Hz pulses in awake rats, with or without the presence of various doses of an N‐methyl‐D‐aspartate (NMDA) receptor antagonist. Apical LTP was blocked by an intracerebroventricular (i.c.v.) dose of 40 μg D‐2‐amino‐5‐phosphonopentanoic acid (D‐AP5) or 20 mg/kg i.p. D‐2‐amino‐4‐methyl‐5‐phosphono‐3‐pentanoic acid (CGP‐40116), whereas basal LTP was blocked by half the dose of D‐AP5 or CGP‐40116. The noncompetitive antagonist MK‐801 (≤1 mg/kg i.p.) had no significant effect on apical LTP. Apical LTP was not blocked by i.c.v. nifedipine. The effect of an NMDA receptor antagonist alone on apical and basal fEPSPs was also evaluated, to assess the net effect of the NMDA receptor antagonist in blocking LTP. MK‐801 (0.5–1 mg/kg i.p.) or CGP‐40116 (10–20 mg/kg i.p.) but not D‐AP5 suppressed apical fEPSPs for several hours and confounded the expression of apical LTP during this time. We concluded that hippocampal LTP at different synapses has different sensitivity to NMDA receptor antagonists and that a general blockade of hippocampal NMDA receptor functions cannot be inferred by a single hippocampal LTP measure. Hippocampus 1999;9:617–630. © 1999 Wiley‐Liss, Inc. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Hippocampus Wiley

N‐methyl‐D‐aspartate receptor antagonists are less effective in blocking long‐term potentiation at apical than basal dendrites in hippocampal CA1 of awake rats

Leung, L. Stan; Shen, Bixia
Hippocampus , Volume 9 (6) – Jan 1, 1999
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References (67)

Publisher
Wiley
Copyright
Copyright © 1999 Wiley Subscription Services
ISSN
1050-9631
eISSN
1098-1063
DOI
10.1002/(SICI)1098-1063(1999)9:6<617::AID-HIPO2>3.0.CO;2-6
pmid
10641754
Publisher site
See Article on Publisher Site

Abstract

Long‐term potentiation (LTP) of field excitatory postsynaptic potentials (fEPSPs) at the apical or basal dendrites of CA1 pyramidal cells was induced by stimulation with a 1‐s train of 200‐Hz pulses in awake rats, with or without the presence of various doses of an N‐methyl‐D‐aspartate (NMDA) receptor antagonist. Apical LTP was blocked by an intracerebroventricular (i.c.v.) dose of 40 μg D‐2‐amino‐5‐phosphonopentanoic acid (D‐AP5) or 20 mg/kg i.p. D‐2‐amino‐4‐methyl‐5‐phosphono‐3‐pentanoic acid (CGP‐40116), whereas basal LTP was blocked by half the dose of D‐AP5 or CGP‐40116. The noncompetitive antagonist MK‐801 (≤1 mg/kg i.p.) had no significant effect on apical LTP. Apical LTP was not blocked by i.c.v. nifedipine. The effect of an NMDA receptor antagonist alone on apical and basal fEPSPs was also evaluated, to assess the net effect of the NMDA receptor antagonist in blocking LTP. MK‐801 (0.5–1 mg/kg i.p.) or CGP‐40116 (10–20 mg/kg i.p.) but not D‐AP5 suppressed apical fEPSPs for several hours and confounded the expression of apical LTP during this time. We concluded that hippocampal LTP at different synapses has different sensitivity to NMDA receptor antagonists and that a general blockade of hippocampal NMDA receptor functions cannot be inferred by a single hippocampal LTP measure. Hippocampus 1999;9:617–630. © 1999 Wiley‐Liss, Inc.

Journal

Hippocampus – Wiley

Published: Jan 1, 1999

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