Involvement of 5-HT7 receptors in serotonergic effects on spike afterpotentials in presumed jaw-closing motoneurons of rats

Brain Res. 2002 Nov 8;954(2):202-11. doi: 10.1016/s0006-8993(02)03286-9.

Abstract

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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • 8-Hydroxy-2-(di-n-propylamino)tetralin / pharmacology
  • Action Potentials* / drug effects
  • Alkaloids
  • Animals
  • Benzophenanthridines
  • Brain Stem / drug effects
  • Brain Stem / physiology*
  • Calcium / metabolism
  • Clozapine / pharmacology
  • Cyclic AMP-Dependent Protein Kinases / antagonists & inhibitors
  • Cyclic AMP-Dependent Protein Kinases / metabolism
  • Electrophysiology
  • Enzyme Inhibitors / pharmacology
  • Isoquinolines / pharmacology
  • Jaw / physiology*
  • Membrane Potentials / drug effects
  • Motor Neurons / drug effects
  • Motor Neurons / physiology*
  • Phenanthridines / pharmacology
  • Pindolol / pharmacology
  • Protein Kinase C / antagonists & inhibitors
  • Protein Kinase C / metabolism
  • Rats
  • Rats, Sprague-Dawley
  • Receptors, Serotonin / drug effects
  • Receptors, Serotonin / physiology*
  • Ritanserin / pharmacology
  • Serotonin / analogs & derivatives*
  • Serotonin / pharmacology
  • Serotonin Antagonists / pharmacology*
  • Serotonin Receptor Agonists / pharmacology*
  • Sulfonamides*

Substances

  • Alkaloids
  • Benzophenanthridines
  • Enzyme Inhibitors
  • Isoquinolines
  • Phenanthridines
  • Receptors, Serotonin
  • Serotonin Antagonists
  • Serotonin Receptor Agonists
  • Sulfonamides
  • Ritanserin
  • alpha-methylserotonin
  • Serotonin
  • 8-Hydroxy-2-(di-n-propylamino)tetralin
  • Pindolol
  • chelerythrine
  • Cyclic AMP-Dependent Protein Kinases
  • Protein Kinase C
  • Clozapine
  • N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide
  • Calcium