Serotonin excitation of facial motoneurons: Receptor subtype characterization

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‐HT 1 agonist 5‐carboxamidotryptamine (5‐CT), the 5‐HT 2 /5‐HT 1c agonist 1‐[2,5‐demethoxy‐4‐methylphenyl]‐2‐aminopropane (DOM), but not the selective 5‐HT 1A 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‐HT 2 / 5‐HT 1c 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.