Neural changes in the auditory cortex of awake guinea pigs after two tinnitus inducers: salicylate and acoustic trauma.
Tinnitus, also called phantom auditory perception, is a major health problem in western countries. As such, a significant amount of effort has been devoted to understanding its mechanisms, including studies in animals wherein a supposed "tinnitus state" can be induced. Here, we studied on the same awake animals the effects of a high-dose of salicylate and of an acoustic trauma both at levels known to induce tinnitus. Recordings of cortical activity (local field potentials) from chronically implanted electrodes in the same animals under each condition allowed direct comparison of the effects of salicylate and trauma (noise trauma was carried out several days after full recovery from salicylate administration). Salicylate induced a systematic and reversible increase in amplitude of cortical responses evoked by tone bursts over a wide range of frequencies and intensities. The effects of noise trauma, though much more variable than those of salicylate, resulted in both increases and decreases in the amplitude of cortical responses. These alterations of cortical response amplitudes likely reflect associated hypoacusis and hyperacusis. The effects of salicylate administration and noise trauma on spontaneous activity were also studied. Fourier analysis did not reveal any increase in power within any given frequency band; rather, both treatments induced a decrease of power spectrum over a relatively broad frequency band (approximately 10-30 Hz). Entropy rate of spontaneous activity, a measure of complexity (temporal correlations), was found to decrease after salicylate but not after acoustic trauma. The present data on evoked potentials confirm salicylate effects at the cortical level and partially extend such effects to acoustic trauma. While the present study showed that both salicylate and noise trauma induced some changes of spontaneous activity in auditory cortex, none of these changes are interpretable in terms of potential neural correlate of tinnitus.
Noreña
A J
AJ
Université de Provence, CNRS UMR 6149, Marseille, France. arnaud.norena@univ-provence.fr
Moffat
G
G
Blanc
J L
JL
Pezard
L
L
Cazals
Y
Y
D000161:Acoustic Stimulation / Q000009:adverse effects; D000200:Action Potentials / Q000187:drug effects / Q000502:physiology; D000818:Animals; D001303:Auditory Cortex / Q000503:physiopathology*; D001306:Auditory Pathways / Q000503:physiopathology; D004195:Disease Models, Animal; D004305:Dose-Response Relationship, Drug; D007758:Ear, Inner / Q000187:drug effects / Q000503:physiopathology*; D005072:Evoked Potentials, Auditory / Q000187:drug effects / Q000502:physiology; D006168:Guinea Pigs; D006198:Hair Cells, Auditory / Q000187:drug effects / Q000473:pathology; D006317:Hearing Loss, Noise-Induced / Q000473:pathology / Q000503:physiopathology*; D012001:Hyperacusis / Q000209:etiology / Q000503:physiopathology; D009498:Neurotoxins / Q000633:toxicity*; D009622:Noise / Q000009:adverse effects; D012459:Salicylates / Q000633:toxicity*; D014012:Tinnitus / Q000209:etiology / Q000503:physiopathology*; D014851:Wakefulness / Q000502:physiology
D009498:Neurotoxins; D012459:Salicylates