title: Gamma-aminobutyric acid circuits shape response properties of auditory cortex neurons.
abstract: Neurons containing gamma aminobutyric acid (GABA) are widely distributed throughout the primary auditory cortex (AI). We investigated the effects of endogenous GABA by comparing response properties of 110 neurons in chinchilla AI before and after iontophoresis of bicuculline, a GABA(A) receptor antagonist, and/or CGP35348, a GABA(B) receptor antagonist. GABA(A) receptor blockade significantly increased spontaneous and driven discharge rates, dramatically decreased the thresholds of many neurons, and constricted the range of thresholds across the neural population. Some neurons with 'non-onset' temporal discharge patterns developed an onset pattern that was followed by a long pause. Interestingly, the excitatory response area typically expanded on both sides of the characteristic frequency; this expansion exceeded one octave in a third of the sample. Although GABA(B) receptor blockade had little effect alone, the combination of CGP35348 and bicuculline produced greater increases in driven rate and expansion of the frequency response area than GABA(A) receptor blockade alone, suggesting a modulatory role of local GABA(B) receptors. The results suggest that local GABA inhibition contributes significantly to intensity and frequency coding by controlling the range of intensities over which cortical neurons operate and the range of frequencies to which they respond. The inhibitory circuits that generate nonmonotonic rate-level functions are separate from those that influence other response properties of AI neurons.
authors.affiliation: Center for Hearing and Deafness, State University of New York at Buffalo, Buffalo, NY 14214, USA.
authors.forename: Jian
authors.initials: J
authors.lastname: Wang
authors.forename: Sandra L
authors.initials: SL
authors.lastname: McFadden
authors.forename: Donald
authors.initials: D
authors.lastname: Caspary
authors.forename: Richard
authors.initials: R
authors.lastname: Salvi
mesh_terms: D000161:Acoustic Stimulation; D000200:Action Potentials / Q000187:drug effects / Q000502:physiology*; D000818:Animals; D001303:Auditory Cortex / Q000166:cytology / Q000187:drug effects / Q000378:metabolism*; D001307:Auditory Perception / Q000187:drug effects / Q000502:physiology*; D001309:Auditory Threshold / Q000187:drug effects / Q000502:physiology; D001640:Bicuculline / Q000494:pharmacology; D002682:Chinchilla; D018756:GABA Antagonists / Q000494:pharmacology; D058787:GABA-A Receptor Antagonists; D058788:GABA-B Receptor Antagonists; D009433:Neural Inhibition / Q000187:drug effects / Q000502:physiology; D009434:Neural Pathways / Q000166:cytology / Q000187:drug effects / Q000378:metabolism*; D009474:Neurons / Q000166:cytology / Q000187:drug effects / Q000378:metabolism*; D009943:Organophosphorus Compounds / Q000494:pharmacology; D011930:Reaction Time / Q000187:drug effects / Q000502:physiology; D018079:Receptors, GABA / Q000187:drug effects / Q000378:metabolism*; D011963:Receptors, GABA-A / Q000378:metabolism; D018080:Receptors, GABA-B / Q000378:metabolism; D009435:Synaptic Transmission / Q000187:drug effects / Q000502:physiology; D005680:gamma-Aminobutyric Acid / Q000378:metabolism*
chemical_list: D018756:GABA Antagonists; D058787:GABA-A Receptor Antagonists; D058788:GABA-B Receptor Antagonists; D009943:Organophosphorus Compounds; D018079:Receptors, GABA; D011963:Receptors, GABA-A; D018080:Receptors, GABA-B; D005680:gamma-Aminobutyric Acid; C066430:CGP 35348; D001640:Bicuculline