RAPID COMMUNICATION Protein Kinase C Activation Decreases Activity-Dependent Attenuation of Dendritic Na Current in Hippocampal CA1 Pyramidal Neurons

Colbert, Costa M. and Daniel Johnston. Protein kinase C activarent because of this inactivation was approximately twofold tion decreases activity-dependent attenuation of dendritic Na curgreater in dendritic patches than somatic patches (Colbert rent in hippocampal CA1 pyramidal neurons. J. Neurophysiol. 79: et al. 1997). Although the K currents did not show any 491–495, 1998. Action potentials recorded from the soma of CA1 activity-dependent changes in amplitude, their presence in pyramidal neurons remain relatively uniform in amplitude during the dendrites at a high density enhanced the effects of Na repetitive firing. In contrast, the amplitudes of back-propagating current attenuation in the dendrites. action potentials in dendrites decrease progressively during a spike What underlies the differences in recovery from inactivatrain. This activity-dependent decrease in amplitude is dependent tion between somatic and dendritic Na channels? No previon the frequency of firing during the train and distance from the ous evidence supports the idea of different channel subtypes: soma. Previously, we described a property of Na channels that provides a plausible mechanism for the activity dependence of the other properties such as conductance, activation, and fast amplitude of the dendritic action potentials: available Na current inactivation are all similar in the soma, dendrites, and initial decreases during trains of action potentials through an inactivation, segment (Colbert and Johnston 1996; Magee and Johnston distinct from fast inactivation, that appears rapid in onset, but slow 1995; Stuart and Sakmann 1994). Thus we wondered and voltage-dependent in its recovery. In this study we found that whether local modulation of Na channels, rather than difactivation of protein kinase C by phorbol esters decreased this ferent types of channels, might determine the regional differactivity-dependent inactivation of pharmacologically isolated Na ences in slow recovery from inactivation. In the present study current in cell-attached dendritic, but not somatic, patches. Simiwe found that phorbol esters decreased both the activitylarly in whole cell recordings phorbol esters decreased the attenuadependent inactivation of dendritic Na channels and the tion of back-propagating dendritic action potentials during trains. decline in spike amplitude during trains of back-propagating These results indicate a novel effect of protein kinase C on the dendritic Na channel and further support the hypothesis that the dendritic action potentials. activity dependence of the dendritic action potentials is derived from the inactivation properties of Na channels. M E T H O D S