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Modulation of Transient and Persistent Inward Currents by Activation of Protein Kinase C in Spinal Ventral Neurons of the Neonatal Rat

Department of Physiology, University of Manitoba, Winnipeg, Manitoba, Canada

Submitted 14 October 2008; accepted in final form 21 October 2008

Neuronal excitability can be regulated through modulation of voltage threshold (V_th). Previous studies suggested that this modulation could be mediated by modulation of transient sodium currents (I_T) and/or persistent inward current (PIC). Modulation of I_T and PIC through activation of protein kinase C (PKC) has previously been described as a mechanism controlling neuronal excitability. We investigated modulation of I_T and PIC by PKC in neonatal rat spinal ventral neurons. In whole cell voltage clamp, activation of PKC by application of 1-oleoyl-2-acetyl-sn-glycerol (OAG, 10–30 µM) resulted in 1) a reduction of I_T amplitude by 33% accompanied an increase in half-width and a decrease in the maximal rise and decay rates of the I_T; 2) a reduction of PIC amplitude by 49%, with a depolarization of PIC onset by 4.5 mV. Activation of PKC caused varied effects on V_th for eliciting I_T, with an unchanged V_th or depolarized V_th being the most common effects. In current-clamp recordings, PKC activation produced a small but significant depolarization (2.0 mV) of V_th for action potential generation with an increase in half-width and a decrease in amplitude and the maximal rise and decay rates of action potentials. Inclusion of PKCI_19–36 (10–30 µM), a PKC inhibitor, in the recording pipette could block the OAG effects on I_T and PIC. The ability of serotonin to hyperpolarize V_th was not altered by PKC activation or inhibition. This study demonstrates that activation of PKC decreases the excitability of spinal ventral neurons and that V_th can be modulated by multiple mechanisms.

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