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The Journal of Neuroscience, June 15, 2000, 20(12):4446-4451
Inhibition of the cAMP Pathway Decreases Early Long-Term
Potentiation at CA1 Hippocampal Synapses
Nonna A.
Otmakhova,
Nikolai
Otmakhov,
Lindsay H.
Mortenson, and
John E.
Lisman
Department of Biology and Volen Center for Complex Systems,
Brandeis University, Waltham, Massachusetts 02454
Long-term potentiation (LTP) has several different phases, and
there is general agreement that the late phase of LTP requires the
activation of adenylyl cyclase (AC) and cAMP-dependent protein kinase (PKA). In contrast, several studies indicate that the early LTP
is not affected by interfering with the cAMP pathway. We have further
tested the role of the cAMP pathway in early LTP using several types of
inhibitors. Bath application of the PKA inhibitor H89 suppressed the
early LTP induced by a single tetanus. Similarly, the LTP induced by a
pairing protocol was decreased by postsynaptic intracellular perfusion
of the peptide PKA inhibitor PKI(6-22) amide. The decrease of LTP
produced by these inhibitors was evident immediately after induction.
These results indicate that PKA is important in early LTP, that its
locus of action is postsynaptic, and that it does not act merely by
enhancing the depolarization required for LTP induction. The
failure of some other inhibitors of the cAMP pathway to affect the
early phase of LTP might be attributable to the saturation of some step
in the cAMP pathway during a tetanus. In agreement with this hypothesis
we found that application of the AC inhibitor SQ 22536 by itself did
not affect the early phase of LTP, but did produce a reduction if the
cAMP pathway was already attenuated by the PKA inhibitor H89. Our
analysis of the results of genetic modifications of the cAMP pathway,
especially the work on AC knock-outs, indicates that the genetic data
are generally consistent with the pharmacological results showing the
importance of this pathway in early LTP.
Key words:
adenylyl cyclase; CA1; cAMP-dependent protein kinase; early LTP; H89; PKI(6-22) amide; SQ 22536
Copyright © 2000 Society for Neuroscience 0270-6474/00/20124446-06$05.00/0
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