TY - JOUR
T1 - Modulation of a transient K+ current in the pleural sensory neurons of Aplysia by serotonin and cAMP
T2 - Implications for spike broadening
AU - Hochner, Binyamin
AU - Kandel, Eric R.
PY - 1992/12/1
Y1 - 1992/12/1
N2 - 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.
AB - 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.
UR - http://www.scopus.com/inward/record.url?scp=0026475198&partnerID=8YFLogxK
U2 - 10.1073/pnas.89.23.11476
DO - 10.1073/pnas.89.23.11476
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C2 - 1333611
AN - SCOPUS:0026475198
SN - 0027-8424
VL - 89
SP - 11476
EP - 11480
JO - Proceedings of the National Academy of Sciences of the United States of America
JF - Proceedings of the National Academy of Sciences of the United States of America
IS - 23
ER -