Auditory sensori-neural alterations induced by salicylate

@article{Cazals2000AuditorySA,
  title={Auditory sensori-neural alterations induced by salicylate},
  author={Yves Cazals},
  journal={Progress in Neurobiology},
  year={2000},
  volume={62},
  pages={583-631}
}
  • Y. Cazals
  • Published 15 December 2000
  • Biology
  • Progress in Neurobiology
Review of salicylate-induced hearing loss, neurotoxicity, tinnitus and neuropathophysiology
TLDR
Current knowledge of salicylate ototoxicity and interactions is discussed, including how acute and chronic dosing affects the peripheral system by causing a compensatory temporary enhancement in DPOAE amplitudes and up-regulation of prestin mRNA and protein expression.
Salicylate toxicity model of tinnitus
TLDR
Some of the intriguing biochemical and physiological effects associated with salicylate-induced tinnitus, some of which occur in the periphery and others in the central nervous system are summarized.
Salicylate-Induced Changes in Hearing Thresholds in Mongolian Gerbils Are Correlated With Tinnitus Frequency but Not With Tinnitus Strength
TLDR
Salicylate-induced tinnitus animals showed no correlation between hearing thresholds and behavioral signs ofTinnitus, indicating that the development of tinnitis after salicylates injection is not based on SR as proposed for the trauma model.
Behavioral Tests for Tinnitus in Animals
TLDR
Interest in tinnitus has increased in recent years, aimed primarily at finding a treatment, but understanding this disorder may also give some insight into the neurological basis of the perception of sound.
Review : Salicylate-Induced Cochlear Impairments , Cortical Hyperactivity and ReTuning , and Tinnitus
TLDR
The results suggest that SS- induced hyperactivity in auditory cortex originates in the central nervous system, that the amygdala potentiates these effects and that the SS-induced tonotopic shifts in auditory cortical, the putative neural correlate of tinnitus, arises from the interaction between the frequency-dependent losses in the cochlea and hyper activity in thecentral nervous system.
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Alterations in average spectrum of cochleoneural activity by long-term salicylate treatment in the guinea pig: a plausible index of tinnitus.
TLDR
The similarities in occurrence, development, reversibility, frequency content, and acoustic level support the idea that ASECA changes, which indicates alterations of spontaneous eighth nerve activity and reflects the presence of salicylate-induced high-pitch tinnitus.
Animal models of tinnitus.
TLDR
Several lines of evidence point to the signal as being cochlear in origin, including: its resistance to muscular paralysis and section of the stapedius muscle; the effects of changes in middle-ear pressure; its reversible elimination by hypoxia; and its suppression by tones of higher frequency.
An animal model of tinnitus: a decade of development.
TLDR
A behavioral model of tinnitus is developed by combining a variety of methodologies, including a behavioral component, to allow for the detection ofTinnitus perception and the discovery of abnormal, epileptic-like, neuronal activity.
Mechanisms of salicylate ototoxicity
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