Ionic basis for plateau potentials in deep dorsal horn neurons of the rat spinal cord.

Approximately 28% of dorsal horn neurons (DHNs) in lamina V of the rat spinal cord generate voltage-dependent plateau potentials underlying accelerating discharges and prolonged afterdischarges in response to steady current pulses or stimulation of nociceptive primary afferent fibers. Using intracellular recordings in a transverse slice preparation of the cervical spinal cord, we have analyzed the ionic mechanisms involved in the generation and maintenance of plateau potentials in lamina V DHNs. Both the accelerating discharges and afterdischarges were reversibly blocked by Mn(2+) and enhanced when Ca(2+) was substituted with Ba(2+). The underlying tetrodotoxin-resistant regenerative depolarization was sensitive to dihydropyridines, being blocked by nifedipine and enhanced by Bay K 8644. Substitution of extracellular Na(+) with N-methyl-D-glucamine or choline strongly decreased the duration of the plateau potential. Loading the neurons with the calcium chelator BAPTA did not change the initial response but clearly decreased the maximum firing frequency and the duration of the afterdischarge. A similar effect was obtained with flufenamate, a specific blocker of the calcium-activated nonspecific cation current (I(CAN)). We conclude that the plateau potential of deep DHNs is supported by both Ca(2+) influx through intermediate-threshold voltage-gated calcium channels of the L-type and by subsequent activation of a CAN current. Ca(2+) influx during the plateau is potentially of importance for pain integration and the associated sensitization in spinal cord.