1. Current and voltage recordings were made from antidromically identified motoneurones
(MNs) in transverse thoracolumbar spinal cord slices of neonatal rats. 2. Applied
by superfusion (10-100 microM) or pressure ejection, 5-hydroxytryptamine (5-HT) elicited
a slow depolarization (or inward current) in 81% and a hyperpolarization (or outward
current) in 9% of responsive MNs; the responses persisted in a low-Ca2+, high-Mg2+
or tetrodotoxin (TTX)-containing solution. 3. 5-HT induced the occurrence in some
MNs of excitatory postsynaptic potentials (EPSPs) or inhibitory postsynaptic potentials
(IPSPs), which were reversibly eliminated by TTX, low-Ca2+, high-Mg2+ solution or
by the 5-HT2 receptor antagonists ketanserin and spiperone. Also, kynurenic acid and
strychnine abolished, respectively, the 5-HT-induced EPSPs and IPSPs. 4. The 5-HT
depolarization was associated with increased membrane resistance, was reduced by hyperpolarization
and nullified near -100 mV. The extrapolated reversal potential was shifted to a positive
direction in elevated [K+]o. 5. The depolarizing response was mimicked by the 5-HT2
receptor agonist (+2-)-1(2,5-dimethyoxy-4-iodophenyl)-2-aminopropane hydrochloride
(DOI) and blocked by 5-HT antagonists methysergide and cyproheptadine and by 5-HT2
antagonists ketanserin and spiperone; methiothepin and MDL 72222 were without effect.
6. The 5-HT hyperpolarization was associated with decreased membrane resistance. The
5-HT1A agonist 8-hydroxy-2-(di-N-propylamino) tetralin hydrobromide (8-OH-DPAT) mimicked
the hyperpolarizing response. 7. Single or repetitive (10-30 Hz) electrical stimuli
elicited in about 30% of MNs, in addition to a fast EPSP, a slow EPSP with electrophysiological
characteristics similar to that of 5-HT induced depolarization. Methysergide and spiperone
abolished the slow EPSPs evoked in some of these MNs. 8. It is suggested that 5-HT,
acting on 5-HT2 and 5-HT1A receptors, depolarizes and hyperpolarizes the MNs by decreasing
and increasing K+ conductance. Additionally, 5-HT activates, via 5-HT2 receptors,
excitatory and inhibitory interneurones, thereby indirectly affecting the activity
of MNs. More importantly, 5-HT released from intraspinal nerves appears to be the
mediator of a slow EPSP in a population of MNs.