title: Cholinergic synaptic potentials in the supragranular layers of auditory cortex.
abstract: Receptive-field plasticity within the auditory neocortex is associated with learning, memory, and acetylcholine (ACh). However, the interplay of elements involved in changing receptive-fields remains unclear. Herein, we describe a depolarizing and a hyperpolarizing potential elicited by repetitive stimulation (20-100 Hz, 0.5-2 sec) and dependent on ACh, which may be involved in modifying receptive-fields. These potentials were recorded, using whole cell techniques, in layer II/III pyramidal cells in the rat auditory cortex in vitro. Stimulation at low stimulus intensities can give rise to a hyperpolarizing response and stimulation at higher stimulus intensities can elicit a depolarizing response. The depolarizing response had a reversal potential of -35 mV, and was reduced by the combination of AMPA/kainate and NMDA 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, GABA(A) receptor antagonists (bicuculline and a Cl(-) channel blocker picrotoxin), and to a small extent a GABA(B) receptor antagonist (saclofen). This suggests that the hyperpolarizing response is likely to be mediated by ACh acting on GABAergic interneurons. Extracellular recordings, also made from layer II/III of cortical slices, yielded a negative-going potential which was reduced by ionotropic glutamate receptor antagonists (same as above) and by the ACh receptor antagonists atropine and scopolamine, suggesting that this potential was the extracellular representation of the depolarizing response.
authors.affiliation: Neuroscience Program, Department of Psychology, University of California, Riverside, California 92521, USA.
authors.forename: A E
authors.initials: AE
authors.lastname: Bandrowski
authors.forename: S L
authors.initials: SL
authors.lastname: Moore
authors.forename: J H
authors.initials: JH
authors.lastname: Ashe
mesh_terms: D000109:Acetylcholine / Q000378:metabolism* / Q000494:pharmacology; D000818:Animals; D001303:Auditory Cortex / Q000166:cytology / Q000187:drug effects / Q000378:metabolism*; D001307:Auditory Perception / Q000187:drug effects / Q000502:physiology; D002799:Cholinergic Fibers / Q000187:drug effects / Q000378:metabolism*; D004558:Electric Stimulation; D004594:Electrophysiology; D018691:Excitatory Amino Acid Antagonists / Q000494:pharmacology; D018756:GABA Antagonists / Q000494:pharmacology; D007395:Interneurons / Q000187:drug effects / Q000378:metabolism; D008297:Male; D018727:Muscarinic Antagonists / Q000494:pharmacology; D009433:Neural Inhibition / Q000187:drug effects / Q000502:physiology; D009473:Neuronal Plasticity / Q000187:drug effects / Q000502:physiology*; D009474:Neurons / Q000187:drug effects / Q000378:metabolism*; D051381:Rats; D017207:Rats, Sprague-Dawley; D017470:Receptors, Glutamate / Q000187:drug effects / Q000378:metabolism; D013569:Synapses / Q000187:drug effects / Q000378:metabolism*; D009435:Synaptic Transmission / Q000187:drug effects / Q000502:physiology*; D005680:gamma-Aminobutyric Acid / Q000378:metabolism
chemical_list: D018691:Excitatory Amino Acid Antagonists; D018756:GABA Antagonists; D018727:Muscarinic Antagonists; D017470:Receptors, Glutamate; D005680:gamma-Aminobutyric Acid; D000109:Acetylcholine