title: Intracortical circuits amplify sound-evoked activity in primary auditory cortex following systemic injection of salicylate in the rat.
abstract: A high dose of sodium salicylate temporarily induces tinnitus, mild hearing loss, and possibly hyperacusis in humans and other animals. Salicylate has well-established effects on cochlear function, primarily resulting in the moderate reduction of auditory input to the brain. Despite decreased peripheral sensitivity and output, salicylate induces a paradoxical enhancement of the sound-evoked field potential at the level of the primary auditory cortex (A1). Previous electrophysiologic studies have begun to characterize changes in thalamorecipient layers of A1; however, A1 is a complex neural circuit with recurrent intracortical connections. To describe the effects of acute systemic salicylate treatment on both thalamic and intracortical sound-driven activity across layers of A1, we applied current-source density (CSD) analysis to field potentials sampled across cortical layers in the anesthetized rat. CSD maps were normally characterized by a large, short-latency, monosynaptic, thalamically driven sink in granular layers followed by a lower amplitude, longer latency, polysynaptic, intracortically driven sink in supragranular layers. Following systemic administration of salicylate, there was a near doubling of both granular and supragranular sink amplitudes at higher sound levels. The supragranular sink amplitude input/output function changed from becoming asymptotic at approximately 50 dB to sharply nonasymptotic, often dominating the granular sink amplitude at higher sound levels. The supragranular sink also exhibited a significant decrease in peak latency, reflecting an acceleration of intracortical processing of the sound-evoked response. Additionally, multiunit (MU) activity was altered by salicylate; the normally onset/sustained MU response type was transformed into a primarily onset response type in granular and infragranular layers. The results from CSD analysis indicate that salicylate significantly enhances sound-driven response via intracortical circuits.
authors.affiliation: Center for Hearing and Deafness, State University of New York at Buffalo, Buffalo, NY 14214, USA. djs32@buffalo.edu
authors.forename: Daniel
authors.initials: D
authors.lastname: Stolzberg
authors.forename: Michael
authors.initials: M
authors.lastname: Chrostowski
authors.forename: Richard J
authors.initials: RJ
authors.lastname: Salvi
authors.forename: Brian L
authors.initials: BL
authors.lastname: Allman
mesh_terms: D000161:Acoustic Stimulation; D000818:Animals; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000494:pharmacology*; D001303:Auditory Cortex / Q000187:drug effects* / Q000502:physiology; D001306:Auditory Pathways / Q000502:physiology*; D004558:Electric Stimulation; D005072:Evoked Potentials, Auditory / Q000187:drug effects* / Q000502:physiology; D008297:Male; D009431:Neural Conduction / Q000187:drug effects; D011571:Psychoacoustics; D051381:Rats; D017207:Rats, Sprague-Dawley; D011930:Reaction Time / Q000187:drug effects; D012459:Salicylates / Q000494:pharmacology*
chemical_list: D000894:Anti-Inflammatory Agents, Non-Steroidal; D012459:Salicylates