title: Cross-modal plasticity results in increased inhibition in primary auditory cortical areas.
abstract: Loss of sensory input from peripheral organ damage, sensory deprivation, or brain damage can result in adaptive or maladaptive changes in sensory cortex. In previous research, we found that auditory cortical tuning and tonotopy were impaired by cross-modal invasion of visual inputs. Sensory deprivation is typically associated with a loss of inhibition. To determine whether inhibitory plasticity is responsible for this process, we measured pre- and postsynaptic changes in inhibitory connectivity in ferret auditory cortex (AC) after cross-modal plasticity. We found that blocking GABAA receptors increased responsiveness and broadened sound frequency tuning in the cross-modal group more than in the normal group. Furthermore, expression levels of glutamic acid decarboxylase (GAD) protein were increased in the cross-modal group. We also found that blocking inhibition unmasked visual responses of some auditory neurons in cross-modal AC. Overall, our data suggest a role for increased inhibition in reducing the effectiveness of the abnormal visual inputs and argue that decreased inhibition is not responsible for compromised auditory cortical function after cross-modal invasion. Our findings imply that inhibitory plasticity may play a role in reorganizing sensory cortex after cross-modal invasion, suggesting clinical strategies for recovery after brain injury or sensory deprivation.
authors.affiliation: Department of Biology, Georgia State University, Atlanta, GA 30303, USA.
authors.forename: Yu-Ting
authors.initials: YT
authors.lastname: Mao
authors.forename: Sarah L
authors.initials: SL
authors.lastname: Pallas
mesh_terms: D000161:Acoustic Stimulation; D000818:Animals; D000831:Animals, Newborn; D001303:Auditory Cortex / Q000187:drug effects / Q000502:physiology*; D001309:Auditory Threshold; D015153:Blotting, Western; D004566:Electrodes; D055724:Electrophysiological Phenomena / Q000502:physiology; D005289:Ferrets / Q000502:physiology*; D018756:GABA Antagonists / Q000494:pharmacology; D005968:Glutamate Decarboxylase / Q000378:metabolism; D007150:Immunohistochemistry; D007245:Inferior Colliculi / Q000502:physiology; D007478:Iontophoresis; D009043:Motor Activity / Q000502:physiology; D009473:Neuronal Plasticity / Q000187:drug effects / Q000502:physiology*; D010775:Photic Stimulation; D011724:Pyridazines / Q000494:pharmacology; D011963:Receptors, GABA-A / Q000187:drug effects; D011984:Sensory Receptor Cells / Q000187:drug effects / Q000502:physiology; D013477:Superior Colliculi / Q000502:physiology
chemical_list: D018756:GABA Antagonists; D011724:Pyridazines; D011963:Receptors, GABA-A; C049853:gabazine; D005968:Glutamate Decarboxylase; C401141:glutamate decarboxylase 2