Serotonin excitation of facial motoneurons: Receptor subtype characterization
Article first published online: 12 OCT 2004
Copyright © 1990 Wiley-Liss, Inc.
Volume 5, Issue 4, pages 324–332, 1990
How to Cite
Rasmussen, K. and Aghajanian, G. K. (1990), Serotonin excitation of facial motoneurons: Receptor subtype characterization. Synapse, 5: 324–332. doi: 10.1002/syn.890050409
- Issue published online: 12 OCT 2004
- Article first published online: 12 OCT 2004
- Manuscript Accepted: 26 JAN 1990
- Manuscript Received: 5 DEC 1989
- Brain slices;
- Facial nucleus;
- 5-HT1 receptors;
- 5-HT2 receptors;
- Intracellular recording;
The receptor subtype (s) mediating the enhancement of facial motoneuron exctitability by serotonin (5-HT) was evaluated by means of single-cell recording in vivo (in the anesthetized rat) and in vitro in brain slices. In vivo, microiontophoretic application of the broad-spectrum 5-HT1 agonist 5-carboxamidotryptamine (5-CT), the 5-HT2/5-HT1c agonist 1-[2,5-demethoxy-4-methylphenyl]-2-aminopropane (DOM), but not the selective 5-HT1A agonist 8-OH-2[di-n-propylamino]tetralin (8-OH-DPAT), produced a 5-HT-like enhancement of facial motoneuron excitability. Intravenous administration of the 5-HT2/ 5-HT1c antagonists ritanserin and LY 53857 in vivo blocked the facilitatory effects of 5-HT and DOM, but not norepinephrine (NE). Similarly, in brain slices, bath application of ritanserin blocked the effects of 5-HT, DOM, and 5-CT, but not NE on facial motoneurons. Intracellular recordings showed that DOM induced a slow depolarization and an increase in evoked spikes, but these effects were of lesser magnitude and longer duration than those produced by 5-HT. Taken together these result indicate a a role for 5-HT2 and/or 5-HT1c but not 5-HT1A receptors in serotonergic enhancement of facial motoneuron excitability since 5-HTs effect was (1) at least partially mimicked by the selective 5-HT2/5-HTlc agonist DOM, (2) mimicked by the broad-spectrum 5-HT1 agonist 5-CT but not the selective 5-HTlA agonist 8-OH-DPAT, and (3) blocked by the 5-HT2/5-HT1c antagonists ritanserin and LY 53857.