GABA-A antagonist causes dramatic expansion of tuning in primary auditory cortex.
Responses from 80 neurons in primary auditory cortex of anesthetized chinchillas were investigated before and during iontophoresis of bicuculline (BIC), a GABA-A antagonist. BIC caused a significant increase in the spontaneous discharge rate (SR) and driven firing rate in most neurons. Threshold decreased in many neurons and the excitatory response area expanded significantly above and below the neuron's characteristic frequency (CF). These results indicate that many neurons in primary auditory cortex receive excitatory inputs from a much broader frequency range than previously believed. GABA-A mediated inhibition can significantly alter the excitability and tuning of auditory cortex and could contribute significantly to cortical plasticity due to experience and cochlear pathology.
Wang
J
J
Hearing Research Laboratory, University at Buffalo, NY 14214, USA.
Caspary
D
D
Salvi
R J
RJ
D000161:Acoustic Stimulation; D000818:Animals; D001303:Auditory Cortex / Q000166:cytology / Q000187:drug effects* / Q000378:metabolism*; D001309:Auditory Threshold / Q000187:drug effects* / Q000502:physiology*; D001640:Bicuculline / Q000494:pharmacology*; D002682:Chinchilla; D018756:GABA Antagonists / Q000494:pharmacology*; D058787:GABA-A Receptor Antagonists; D009473:Neuronal Plasticity / Q000187:drug effects* / Q000502:physiology; D009474:Neurons / Q000187:drug effects* / Q000378:metabolism*; D011963:Receptors, GABA-A / Q000378:metabolism; D005680:gamma-Aminobutyric Acid / Q000378:metabolism
D018756:GABA Antagonists; D058787:GABA-A Receptor Antagonists; D011963:Receptors, GABA-A; D005680:gamma-Aminobutyric Acid; D001640:Bicuculline