SLOW RECOVERY FROM INACTIVATION OF NA-DEPENDENT ATTENUATION OF DENDRITIC ACTION-POTENTIALS IN HIPPOCAMPAL CA1 PYRAMIDAL NEURONS( CHANNELS UNDERLIES THE ACTIVITY)

Na+ action potentials propagate into the dendrites of pyramidal neuron s driving an influx of Ca2+ that seems to be important for associative synaptic plasticity. During repetitive (10-50 Hz) firing, dendritic a ction potentials display a marked and prolonged voltage-dependent decr ease in amplitude. Such a decrease is not apparent in somatic action p otentials. We investigated the mechanisms of the different activity de pendence of somatic and dendritic action potentials in CA1 pyramidal n eurons of adult rats using whole-cell and cell-attached patch-clamp me thods. There were three main findings. First, dendritic Na+ currents d ecreased in amplitude when repeatedly activated by brief (2 msec) depo larizations. Recovery was slow and voltage-dependent. Second, Na+ curr ents decreased much less in somatic than in dendritic patches. Third, although K+ currents remained constant during trains, K+ currents were necessary for dendritic action potential amplitude to decrease in who le-cell experiments. These results suggest that regional differences i n Na+ and K+ channels determine the differences in the activity depend ence of somatic and dendritic action potential amplitudes.