Involvement of 5-HT7 receptors in serotonergic effects on spike afterpotentials in presumed jaw-closing motoneurons of rats.
Intracellular recordings were obtained from rat presumed jaw-closing motoneurons in slice preparations to investigate the involvement of the serotonin(7) (5-HT(7)) receptors in serotonergic inhibition of the postspike medium-duration afterhyperpolarization (mAHP) and enhancement of the afterdepolarization (ADP). 5-HT-induced suppression of the mAHP and enhancement of the ADP were mimicked by application of the 5-HT(1A/7) receptor agonist 8-hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT) and antagonized by the 5-HT(2/6/7) receptor antagonist clozapine, whereas the 5-HT(2) receptor agonist alpha-methyl-5-hydroxytryptamine (alpha-methyl-5-HT) did not affect the mAHP and ADP. 8-OH-DPAT-induced attenuation of the mAHP and enhancement of the ADP were also antagonized by clozapine and another 5-HT(2/6/7) receptor antagonist ritanserin, whereas the 5-HT(1A) receptor antagonist pindolol failed to block the 8-OH-DPAT-induced effects on the mAHP and ADP. 8-OH-DPAT-induced suppression of the mAHP and enhancement of the ADP were also antagonized by a protein kinase A (PKA) inhibitor H89, whereas 8-OH-DPAT could inhibit the mAHP and enhance the ADP in the presence of a protein kinase C (PKC) inhibitor chelerythrine. The 8-OH-DPAT-induced suppression of the mAHP was enhanced under raised [Ca(2+)](o) and this enhancement was reduced by chelerythrine. It is suggested that the 5-HT(7) receptors are involved in 5-HT-induced attenuation of the mAHP and enhancement of the ADP through activation of PKA, and the attenuation of mAHP through the 5-HT(7) receptors is enhanced under raised [Ca(2+)](o) by PKC activation.
Inoue
Tomio
T
Department of Oral Physiology, Showa University School of Dentistry, Tokyo 142-8555, Japan. inouet@dent.showa-u.ac.jp
Itoh
Satsuki
S
Wakisaka
Satoshi
S
Ogawa
Satoshi
S
Saito
Mitsuru
M
Morimoto
Toshifumi
T
D017371:8-Hydroxy-2-(di-n-propylamino)tetralin / Q000494:pharmacology; D000200:Action Potentials / Q000187:drug effects; D000470:Alkaloids; D000818:Animals; D053119:Benzophenanthridines; D001933:Brain Stem / Q000187:drug effects / Q000502:physiology*; D002118:Calcium / Q000378:metabolism; D003024:Clozapine / Q000494:pharmacology; D017868:Cyclic AMP-Dependent Protein Kinases / Q000037:antagonists & inhibitors / Q000378:metabolism; D004594:Electrophysiology; D004791:Enzyme Inhibitors / Q000494:pharmacology; D007546:Isoquinolines / Q000494:pharmacology; D007568:Jaw / Q000502:physiology*; D008564:Membrane Potentials / Q000187:drug effects; D009046:Motor Neurons / Q000187:drug effects / Q000502:physiology*; D010617:Phenanthridines / Q000494:pharmacology; D010869:Pindolol / Q000494:pharmacology; D011493:Protein Kinase C / Q000037:antagonists & inhibitors / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D011985:Receptors, Serotonin / Q000187:drug effects / Q000502:physiology*; D016713:Ritanserin / Q000494:pharmacology; D012701:Serotonin / Q000031:analogs & derivatives* / Q000494:pharmacology; D012702:Serotonin Antagonists / Q000494:pharmacology*; D017366:Serotonin Receptor Agonists / Q000494:pharmacology*; D013449:Sulfonamides
D000470:Alkaloids; D053119:Benzophenanthridines; D004791:Enzyme Inhibitors; D007546:Isoquinolines; D010617:Phenanthridines; D011985:Receptors, Serotonin; D012702:Serotonin Antagonists; D017366:Serotonin Receptor Agonists; D013449:Sulfonamides; D016713:Ritanserin; C042390:alpha-methylserotonin; D012701:Serotonin; D017371:8-Hydroxy-2-(di-n-propylamino)tetralin; D010869:Pindolol; C016299:chelerythrine; D017868:Cyclic AMP-Dependent Protein Kinases; D011493:Protein Kinase C; D003024:Clozapine; C063509:N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide; D002118:Calcium