A GABA A MEDIATED AFTERDEPOLARIZATION IN PYRAMIDAL NEURONS FROM RAT NEOCORTEX. Cerne, R. and W. J. Spain. Veterans Affairs Puget Sound Health Care System, Seattle, WA 98108 and the Departments of Neurology and Physiology & Biophysics, University of Washington School of Medicine, Seattle, WA 98195.
APStracts 3:0244N, 1996.
We report a novel slow afterdepolarization (sADP) in layer V pyramidal neurons when brain slices from somatosensory cortex are perfused with GABA. Whole-cell recordings were made from visually-identified neurons in slices from 3 to 5 week old rats. The firing of action potentials at 100 Hz for 1 second, evoked by a train of brief current pulses, is typically followed by a slow afterhyperpolarization (sAHP). When GABA (1 mM) was applied to the perfusate, the sAHP was replaced by a sADP of nearly equal to 18 mV in amplitude, which on average lasted for 26 seconds. The sADP was not evoked or terminated as an all-or-none event: it grew in amplitude and duration as the number of evoked action potentials was increased; and when the sADP was interrupted with hyperpolarizing current steps, its amplitude and duration were graded in a time and voltage dependent manner. The sADP did not depend on Ca 2+ entry into the cell: it could be evoked when bath Ca 2+ was replaced by Mn 2+ or in neurons dialyzed with 20 mM BAPTA. We hypothesized that the sADP was predominantly generated in the dendrites because it was associated with the firing of small-amplitude action potentials which continued after the somatic membrane potential was repolarized to -70 mV by steady current injection. We tested this hypothesis by evoking the sADP in neurons with surgically amputated apical dendrites. In those neurons the average duration of the sADP was 78% shorter then in neurons with an intact apical dendrite and there were no associated small action potentials. The sADP was also evoked by muscimol, but not by baclofen, and was blocked by bicuculline or picrotoxin but not by CGP 35348 indicating that it is mediated through the activation of GABA A receptors. Our results suggest that intense activity in the presence of GABA results in a long lasting enhancement of excitability in the apical dendrite which could in turn lead to amplification of distal excitatory synaptic potentials.

Received 17 October 1996; accepted in final form 21 October 1996.
APS Manuscript Number J528-6.
Article publication pending J. Neurophysiol.
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 13 November 1996