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Long-Lasting Increase in Cellular Excitability Associated With the Priming of LTP Induction in Rat Hippocampus
Department of Psychology and the Neuroscience Research Centre, University of Otago, Dunedin, New Zealand Cohen, Akiva S., Christine M. Coussens, Clarke R. Raymond, and Wickliffe C. Abraham. Long-Lasting Increase in Cellular Excitability Associated With the Priming of LTP Induction in Rat Hippocampus...
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Published in: | Journal of neurophysiology 1999-12, Vol.82 (6), p.3139-3148 |
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Main Authors: | , , , |
Format: | Article |
Language: | English |
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Summary: | Department of Psychology and the Neuroscience Research Centre,
University of Otago, Dunedin, New Zealand
Cohen, Akiva S.,
Christine M. Coussens,
Clarke R. Raymond, and
Wickliffe C. Abraham.
Long-Lasting Increase in Cellular Excitability Associated With
the Priming of LTP Induction in Rat Hippocampus. J. Neurophysiol. 82: 3139-3148, 1999. The mechanisms
underlying the facilitation (priming) of long-term potentiation (LTP)
by prior activation of metabotropic glutamate receptors (mGluRs) were
investigated in area CA1 of rat hippocampal slices. In particular, we
focused on whether a long-lasting increase in postsynaptic excitability
could account for the facilitated LTP. Administration of the mGluR
agonist 1S,3R-aminocyclopentanedicarboxylic acid (ACPD) produced rapid
decreases in the amplitude of both the slow spike
afterhyperpolarization (AHP slow ) and spike frequency adaptation recorded intracellularly from CA1 pyramidal cells. These
changes persisted after drug washout, showing only a slow decay over 20 min. ACPD also caused a leftward shift of the field EPSP-population
spike relation and an overall increase in population spike amplitude,
but this effect was not as persistent as the intracellularly measured
alterations in cell excitability. ACPD-treated cells showed increased
spike discharges during LTP-inducing tetanic stimulation, and the
amplitude of the AHP slow was negatively correlated with the
degree of initial LTP induction. The -adrenergic agonist isoproterenol also caused excitability changes as recorded
intracellularly, whereas in extracellular experiments it weakly primed
the induction but not the persistence of LTP. ACPD primed both LTP
measures. Isoproterenol administration during the tetanus occluded the
priming effect of ACPD on initial LTP induction but not its effect on LTP persistence. We conclude that the persistent excitability changes
elicited by ACPD contributes to the priming of LTP induction but that
other ACPD-triggered mechanisms must account for the facilitated
persistence of LTP in the priming paradigm. |
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ISSN: | 0022-3077 1522-1598 |
DOI: | 10.1152/jn.1999.82.6.3139 |