Restraint stress and protection from acoustic injury in mice

  title={Restraint stress and protection from acoustic injury in mice},
  author={Yong Wang and M. Charles Liberman},
  journal={Hearing Research},
Protecting against noise trauma by lateral efferent activation
The activation of the lateral efferent system by sound conditioning is believed to protect against excitotoxicity at the afferent dendrites beneath the inner hair cells, and thereby protect against acoustic overstimulation.
Acute restraint stress alters sound-evoked neural responses in the rat auditory cortex
Preconditioning by the inhalation of pure oxygen protects rat’s cochlear function against noise-induced hearing loss.
The preconditioning successfully protected the rats’ hearing by maximizing and developing tolerance to ischemia and hypoxia caused by the noise by significantly reduced the ABR threshold shifts and restored the amplitudes of DPOAE.
Glucocorticoid receptor and nuclear factor-kappa B interactions in restraint stress-mediated protection against acoustic trauma.
RS protects the cochlea from acoustic trauma by increasing corticosterone and activating GRs, and emphasis how GR activity modulates hearing sensitivity and its importance for the rationale use of glucocorticoids in inner ear diseases.
Glucocorticoid receptor and mitogen-activated protein kinase activity after restraint stress and acoustic trauma.
A GR-dependent ERK-mediated pathway that modulates auditory function after RS and acoustic trauma is demonstrated and reveals new mechanisms that underlie hearing loss and will have implications for the development of pharmacological strategies for protecting against acoustic trauma.
Effect of chronic restraint stress on inhibitory gating in the auditory cortex of rats
Most of the AC neurons showed a weaker response to the second tone than to the first tone, reflecting an IG of the repeated input, which was diminished following chronic restraint stress at both, the single-unit and LFP level.
The Effects of Normobaric Hyperoxia Pre- and Post-treatment on the Development of Noise-Induced Hearing Loss in Rats
Pre- and post-treatment with normobaric hyperoxia seem to produce protectiveects through either boosting cellular oxygenation or maximizing antioxidant enzyme activities and tolerance against noise-induced ischemia and hypoxia in the cochlea against NIHL.


Conditioning-related protection from acoustic injury: effects of chronic deefferentation and sham surgery.
The results from the surgical groups showed that total loss of the OCB significantly increased the noise-induced PTS, whereas Loss of the COCB only did not; that the conditioning exposure in deefferented animals increased, rather than decreased, the PTS from the traumatic exposure; and that animals undergoing sham surgery appeared protected whether or not they received the conditioning noise exposure.
Heat Stress and Protection from Permanent Acoustic Injury in Mice
Results are consistent with the idea that upregulation of heat shock proteins protects the ear from acoustic injury, and suggest that heat stress protection disappeared when the treatment-trauma interval surpassed 24 hr.
The effect of methylprednisolone on acoustic trauma.
The present results indicate that mPSL possesses a therapeutic effect in cases of mild acoustic overstimulation.
Metallothionein Induction in Response to Restraint Stress
Data indicate that glucocorticoid is the primary physiological factor responsible for MT induction following restraint stress, and the glucoc Corticoid receptor is the major transcription factor involved in this process.
A Radical Demise: Toxins and Trauma Share Common Pathways in Hair Cell Death
ABSTRACT: The pathologic similarities noted after ototoxic and/or traumatic injury to the cochlea as well as the key features of the cochlea that make it susceptible to reactive oxygen species (ROS)