Receptive-field plasticity within the auditory neocortex is associated with
learning, memory, and acetylcholine (ACh). However, the interplay of eleme
nts involved in changing receptive-fields remains unclear. Herein, we descr
ibe a depolarizing and a hyperpolarizing potential elicited by repetitive s
timulation (20-100 Hz, 0.5-2 sec) and dependent on ACh, which may be involv
ed in modifying receptive-fields. These potentials were recorded, using who
le cell techniques, in layer II/III pyramidal cells in the rat auditory cor
tex in vitro. Stimulation at low stimulus intensities can give rise to a hy
perpolarizing response and stimulation at higher stimulus intensities can e
licit a depolarizing response. The depolarizing response had a reversal pot
ential of -35 mV, and was reduced by the combination of AMPA/kainate and NM
DA glutamate receptor antagonists (AMPA/kainate: CNQX, DNQX, and GYKI 52466
; NMDA: APV, MK-801) and by the muscarinic ACh receptor antagonist atropine
. The hyperpolarizing response had a reversal potential of -73 mV and could
be reduced by atropine, GABAA receptor antagonists (bicuculline and a Cl-
channel blocker picrotoxin), and to a small, extent a GABAB receptor antago
nist (saclofen). This suggests that the hyperpolarizing response is likely
to be mediated by ACh acting on GABAergic interneurons. Extracellular recor
dings, also made from layer II/III of cortical slices, yielded a negative-g
oing potential which was reduced by ionotropic glutamate receptor antagonis
ts (same as above) and by the ACh receptor antagonists atropine and scopola
mine, suggesting that this potential was the extracellular representation o
f the depolarizing response. (C) 2001 Wiley-Liss, Inc.