Postnatal emergence of serotonin-induced plateau potentials in commissural interneurons of the mouse spinal cord

Abbinanti MD, Zhong G, Harris-Warrick RM. Postnatal emergence of serotonin-induced plateau potentials in commissural interneurons of the mouse spinal cord. J Neurophysiol 108: 2191-2202, 2012. First published July 25, 2012; doi:10.1152/jn.00336.2012.-Most studies of the mouse hindlimb locomotor network have used neonatal (P0-5) mice. In this study, we examine the postnatal development of intrinsic properties and serotonergic modulation of intersegmental commissural interneurons (CINs) from the neonatal period (P0-3) to the time the animals bear weight (P8-10) and begin to show adult walking (P14-16). CINs show an increase in excitability with age, associated with a decrease in action potential halfwidth and appearance of a fast component to the afterhyperpolarization at P14-16. Serotonin (5-HT) depolarizes and increases the excitability of most CINs at all ages. The major developmental difference is that serotonin can induce plateau potential capability in P14-16 CINs, but not at younger ages. These plateau potentials are abolished by nifedipine, suggesting that they are mediated by an L-type calcium current, I-Ca(L). Voltage-clamp analysis demonstrates that 5-HT increases a nifedipine-sensitive voltage-activated calcium current, I-Ca(V), in P14-16 CINs but does not increase I-Ca(V) in P8-10 CINs. These results, together with earlier work on 5-HT effects on neonatal CINs, suggest that 5-HT increases the excitability of CINs at all ages studied, but by opposite effects on calcium currents, decreasing N- and P/Q-type calcium currents and, indirectly, calcium-activated potassium current, at P0-3 but increasing I-Ca(L) at P14-16.