Rapid kinetics and inward rectification of miniature EPSCs in layer I neurons of rat neocortex. Fu-Ming Zhou and John J. Hablitz. Neurobiology Research Center and Department of Physiology and Biophysics, University of Alabama at Birmingham, Birmingham, AL 35294, USA.
APStracts 4:0037N, 1997.
ABSTRACT
Using the whole-cell patch clamp technique combined with visualization of neurons in brain slices, we have studied the properties of miniature excitatory postsynaptic currents (mEPSCs) in rat neocortical layer I neurons. At holding potentials (-50 to -70 mV) near the resting membrane potential (RMP), mEPSCs had amplitudes of 5 to 100 pA and were mediated mostly by (- amino-3-hydroxy-5-methyl-4-isoxazoleproprionate (AMPA) receptors. Amplitude histograms were skewed toward large events. An NMDA component was revealed by depolarization to -30 mV or using a Mg2+-free bathing solution. At RMP, averaged AMPA mEPSCs had a 10-90% rise time of about 0.3 ms (uncorrected for instrument filtering). The decay of averaged mEPSCs was best fit by double exponential functions in most cases. The fast, dominating component had a decay time constant of about 1.2 ms and comprised about 80% of the total amplitude. A small slow component had a decay time constant of about 4 ms. Positive correlations were found between rise and decay times of both individual and averaged mEPSCs, indicative of dendritic filtering. Some large amplitude mEPSCs and spontaneous EPSCs (recorded in the absence of TTX) had slower kinetics, suggesting a role of asynchronous transmitter release in shaping EPSCs. The amplitudes of mEPSCs were much smaller at +60 than at -60 mV, indicating that synaptic AMPA receptor-mediated currents were inwardly rectifying. These results suggest that neocortical layer I neurons receive both NMDA and AMPA receptor-mediated synaptic inputs. The rapid decay of EPSCs appears to be largely determined by AMPA receptor deactivation. The observed rectification of synaptic responses suggest that synaptic AMPA receptors in layer I neurons may lack GluR-2 subunits and be Ca2+ permeable. 

Received 9 August 1996; accepted in final form 7 January 1997.
APS Manuscript Number J633-6.
Article publication pending J. Neurophysiol.
ISSN 1080-4757 Copyright 1997 The American Physiological Society.
Published in APStracts on 5 February 1997