FIG. 3.

Persistent sodium current (Na PIC) in motoneurons is facilitated by the 5-HT₂ receptor agonist (±)-1-(2,5-dime-thoxy-4-iodophenyl)-2-aminopropane (DOI), and motoneurons of chronic spinal rats are supersensitive to DOI. All recordings (A–D) done in 15 µM nimodipine to block persistent calcium current (Ca PIC; see methods). A: in acute spinal rat motoneuron, high-dose DOI (30 µM) facilitated the Na PIC and hyperpolarized Na PIC onset (V_START; arrowheads: black: control; white: DOI). Same format as in Fig. 1A. B: in motoneuron after chronic injury, Na PIC amplitude was increased and PIC onset hyperpolarized by DOI. C: leak-subtracted current-voltage (I–V) curves of acute spinal rat motoneurons in nimodipine (control), after DOI application and after TTX application. Na PIC induced by high-dose DOI was subsequently blocked by tetrodotoxin (TTX). D: current induced by DOI (I–V curve in nimodipine subtracted from I–V curve in nimodipine + DOI). For chronic spinal rat motoneurons, higher doses of DOI induce larger increases in Na PIC amplitude (dose-dependent). Effect of high dose (≥30 µM) DOI in acute spinal rats was similar to low dose (≤10 µM) in chronic spinal rats. E: group data for DOI effect on Na PIC, measured in nimodipine. Significant effect of DOI for chronic spinal rat motoneurons at all doses tested. Only high doses (≥30 µM) were effective in acute spinal rat motoneurons. Asterisk (*) indicates significant effect of DOI.