Stress induces transient auditory hypersensitivity in rats.
Exposure to harsh environment induces stress reactions that increase probability of survival. Stress influences the endocrine, nervous and immune systems and affects the functioning of a variety of organs. Numerous researchers demonstrated that a 24-h exposure to an acoustic rodent repellent provokes stress reaction in exposed animals. In addition to the activated hypothalamic-pituitary-adrenal (HPA) axis, exposed animals had pathological reactions in the reproductive organs, bronchia and skin. Here, we examined the effect of above stress model on the auditory system of Wistar rats. We found that 24-h stress decreases the thresholds and increases the amplitudes of auditory brainstem responses and distortion product otoacoustic emissions. Resultant auditory hypersensitivity was transient and most pronounced between 3 and 6h post-stress, returning to control levels one week later. The concentration of corticosterone and tumor necrosis factor alpha was systemically elevated in stressed animals between 3 and 6h post-stress, confirming the activation of the HPA axis. In addition, expression of the HPA-axis-associated genes: glucocorticoid receptor (GR) and hypoxia-inducible factor 1 alpha (Hif1a) was modulated in the auditory tissues. In detail, in the inferior colliculus, we found an up-regulation of GR mRNA 3h post-stress and continuous up-regulation of Hif1a up to 24h post-stress. In the spiral ganglion, we found no differences in gene expression between stressed and control animals. In the organ of Corti, expression of GR mRNA remained stable, whereas that of Hif1a was significantly down-regulated one week after stress. In addition, the expression of an outer hair cell marker prestin was significantly up-regulated 6h post-stress. We conclude that 24-h stress induces transient hypersensitivity of the auditory system and modulates gene expression in a tissue-specific manner. Stress-induced auditory hypersensitivity could have evolutionary consequence by giving animals an advantage of hearing better under stress conditions.
Molecular Biology Research Laboratory, Department of Otorhinolaryngology, Charité - Universitätsmedizin Berlin, Berlin, Germany. birgit.mazurek@charite.de
Birgit
B
Mazurek
Heidemarie
H
Haupt
Ricarda
R
Joachim
Burghard F
BF
Klapp
Timo
T
Stöver
Agnieszka J
AJ
Szczepek
D000818:Animals; D001309:Auditory Threshold / Q000502:physiology*; D001483:Base Sequence; D005075:Biological Evolution; D003345:Corticosterone / Q000097:blood; D016207:Cytokines / Q000097:blood; D017931:DNA Primers / Q000235:genetics; D016057:Evoked Potentials, Auditory, Brain Stem / Q000502:physiology; D005260:Female; D015870:Gene Expression; D018072:Hair Cells, Auditory, Outer / Q000502:physiology; D007030:Hypothalamo-Hypophyseal System / Q000502:physiology; D051795:Hypoxia-Inducible Factor 1, alpha Subunit / Q000235:genetics; D007245:Inferior Colliculi / Q000502:physiology; D009925:Organ of Corti / Q000502:physiology; D017084:Otoacoustic Emissions, Spontaneous / Q000502:physiology; D010913:Pituitary-Adrenal System / Q000502:physiology; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D011965:Receptors, Glucocorticoid / Q000235:genetics; D013312:Stress, Physiological / Q000502:physiology*; D013997:Time Factors
D016207:Cytokines; D017931:DNA Primers; C497444:Hif1a protein, rat; D051795:Hypoxia-Inducible Factor 1, alpha Subunit; D012333:RNA, Messenger; D011965:Receptors, Glucocorticoid; D003345:Corticosterone