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ARTICLE, Cellular/Molecular

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
Journal of Neuroscience 15 June 2000, 20 (12) 4446-4451; DOI: https://doi.org/10.1523/JNEUROSCI.20-12-04446.2000
Nonna A. Otmakhova
1Department of Biology and Volen Center for Complex Systems, Brandeis University, Waltham, Massachusetts 02454
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Nikolai Otmakhov
1Department of Biology and Volen Center for Complex Systems, Brandeis University, Waltham, Massachusetts 02454
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Lindsay H. Mortenson
1Department of Biology and Volen Center for Complex Systems, Brandeis University, Waltham, Massachusetts 02454
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John E. Lisman
1Department of Biology and Volen Center for Complex Systems, Brandeis University, Waltham, Massachusetts 02454
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Abstract

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.

  • adenylyl cyclase
  • CA1
  • cAMP-dependent protein kinase
  • early LTP
  • H89
  • PKI(6–22) amide
  • SQ 22536
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The Journal of Neuroscience: 20 (12)
Journal of Neuroscience
Vol. 20, Issue 12
15 Jun 2000
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Inhibition of the cAMP Pathway Decreases Early Long-Term Potentiation at CA1 Hippocampal Synapses
Nonna A. Otmakhova, Nikolai Otmakhov, Lindsay H. Mortenson, John E. Lisman
Journal of Neuroscience 15 June 2000, 20 (12) 4446-4451; DOI: 10.1523/JNEUROSCI.20-12-04446.2000

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Inhibition of the cAMP Pathway Decreases Early Long-Term Potentiation at CA1 Hippocampal Synapses
Nonna A. Otmakhova, Nikolai Otmakhov, Lindsay H. Mortenson, John E. Lisman
Journal of Neuroscience 15 June 2000, 20 (12) 4446-4451; DOI: 10.1523/JNEUROSCI.20-12-04446.2000
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Keywords

  • adenylyl cyclase
  • CA1
  • cAMP-dependent protein kinase
  • early LTP
  • H89
  • PKI(6–22) amide
  • SQ 22536

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