No evidence for enhanced noise induced hearing loss after prenatal stress or dexamethasone.

It was recently implied that prenatal stress and fetal exposure to glucocorticoids may interfere with hearing ability and noise induced hearing loss in adulthood. In the present study pregnant Wistar rats were stressed during gestation by Chronic Mild Stress (CMS, a variable schedule of different stressors) or by dexamethasone (a synthetic glucocorticoid, i.e. a pharmacological stressor). At birth, but not at weaning, the dexamethasone offspring exhibited significantly decreased body weight compared to both control offspring and progeny from dams exposed to CMS during pregnancy. As adults, male offspring were exposed to 105 dB sound pressure level (SPL) wide band noise either continuously for eight hours or for two hours per day on three consecutive days. Oto-acoustic emissions and auditory brainstem responses were recorded before and after exposure to noise. Neither prenatal chronic stress nor prenatal dexamethasone exposure was associated with significantly enhanced noise induced hearing loss compared to controls, and these results were consistent in both subsets of animals. Our data do not support previous reports that prenatal exposure to mild stress nor to dexamethasone is detrimental to the hearing organ per se. However, hearing may be modulated by prenatal stressors under certain circumstances, of which the timing and degree are probably the most important.

Prenatal stress may increase vulnerability to life events: comparison with the effects of prenatal dexamethasone.

Prenatal stress has been associated with a variety of alterations in the offspring. The presented observations suggest that rather than causing changes in the offspring per se, prenatal stress may increase the organism's vulnerability to aversive life events. Offspring of rat dams stressed gestationally by chronic mild stress (CMS, a variable schedule of different stressors) or dexamethasone (DEX, a synthetic glucocorticoid, i.e., a pharmacological stressor) was tested for reactivity by testing their acoustic startle response (ASR). Two subsets of offspring were tested. One was experimentally naïve at the time of ASR testing, whereas the other had been through blood sampling for assessment of the hormonal stress response to restraint, 3 months previously. Both prenatal CMS and dexamethasone increased ASR in the offspring compared to controls, but only in prenatally stressed offspring that had been blood sampled 3 months previously. In conclusion, similarity of the effects of maternal gestational exposure to a regular stress schedule and of exposure to a synthetic glucocorticoid suggests that maternal glucocorticoids may be a determining factor for changes in the regulatory mechanisms of the acoustic startle response. Further, a single aversive life event showed capable of changing the reactivity of prenatally stressed offspring, whereas offspring of dams going through a less stressful gestation was largely unaffected by this event. This suggests that circumstances dating back to the very beginning of life affect the individual's sensitivity towards experiences in life after birth. The prenatal environment may thus form part of the explanation of the considerable individual variation in the development of psychopathology.