Modulation of a transient K+ current in the pleural sensory neurons of Aplysia by serotonin and cAMP: Implications for spike broadening

Binyamin Hochner*, Eric R. Kandel

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

80 Scopus citations

Abstract

To study the contribution of cAMP to the spike broadening produced by serotonin (5-HT) in the pleural sensory neurons of the tail withdrawal reflex, we utilized two phosphodiesterase-resistant cAMP analogs: the SP diastereomer of cyclic adenosine 3′,5′-monophosphothioate (SP-CAMP[S]), which activates protein kinase A, and the antagonist RP diastereomer of cyclic adenosine 3′,5′-monophosphothioate (RP-cAMP[S]), which is a competitive inhibitor of kinase A. When the cAMP agonist SP-cAMP[S] was injected into the sensory neurons, it caused spike broadening comparable to that induced by 5-HT. In turn, the cAMP antagonist RP-cAMP[S] blocked ≈50% of the 5-HT-induced spike broadening. We next examined the K+ currents that are modulated by 5-HT and determined how these currents are affected by cAMP. Confirming Baxter and Byrne [(1989) J. Neurophysiol. 62, 665-679], we found that 5-HT modulated two currents, an S-type K+ current (IKS) as well as a transient and voltage-dependent K+ current (IKV)• RP-cAMP[S] blocked the reduction by 5-HT of the early phase of IKV in parallel with, and to the same degree (60%), as this inhibitor blocked the IKS and spike broadening. These results support the idea that in the pleural sensory neurons cAMP mediates a significant part of the spike broadening that accompanies short-term facilitation produced by 5-HT and that cAMP can produce spike broadening by modulating both IKV and IKS.

Original languageEnglish
Pages (from-to)11476-11480
Number of pages5
JournalProceedings of the National Academy of Sciences of the United States of America
Volume89
Issue number23
DOIs
StatePublished - 1 Dec 1992

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