The Journal of Neurophysiology Vol. 77 No. 2 February 1997, pp. 1039-1045
Copyright ©1997 The American Physiological Society

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GABA_A Mediated Afterdepolarization in Pyramidal Neurons From Rat Neocortex

R. Cerne and W. J. Spain

Veterans Affairs Puget Sound Health Care System, Seattle 98108; and Departments of Neurology and Physiology and Biophysics, University of Washington School of Medicine, Seattle, Washington 98195

Cerne, R. and W. J. Spain. A GABA_A mediated afterdepolarization in pyramidal neurons from rat neocortex. J. Neurophysiol. 77: 1039-1045, 1997. We report a novel slow afterdepolarization (sADP) in layer V pyramidal neurons when brain slices from somatosensory cortex are perfused with -aminobutyric acid (GABA). Whole cell recordings were made from visually identified neurons in slices from 3- to 5-wk-old rats. The firing of action potentials at 100 Hz for 1 s, evoked by a train of brief current pulses, typically is followed by a slow afterhyperpolarization (sAHP). When GABA (1 mM) was applied to the perfusate, the sAHP was replaced by a sADP of 18 mV in amplitude, which on average lasted for 26 s. 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 Ca²⁺ entry into the cell: it could be evoked when bath Ca²⁺ was replaced by Mn²⁺ or in neurons dialyzed with 20 mM bis-(o-aminophenoxy)-N,N,N,N-tetraacetic acid. We hypothesized that the sADP was generated predominantly in the dendrites because it was associated with the firing of small-amplitude action potentials that 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 than in neurons with an intact apical dendrite and there were no associated small action potentials. The sADP also was 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 that in turn could lead to amplification of distal excitatory synaptic potentials.

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