Reversible inactivation of the auditory thalamus disrupts HPA axis habituation to repeated loud noise stress exposures.

Although habituation to stress is a widely observed adaptive mechanism in response to repeated homotypic challenge exposure, its brain location and mechanism of plasticity remains elusive. And while habituation-related plasticity has been suggested to take place in central limbic regions, recent evidence suggests that sensory sites may provide the underlying substrate for this function. For instance, several brainstem, midbrain, thalamic, and/or cortical auditory processing areas, among others, could support habituation-related plasticity to repeated loud noise exposures. In the present study, the auditory thalamus was tested for its putative role in habituation to repeated loud noise exposures, in rats. The auditory thalamus was inactivated reversibly by muscimol injections during repeated loud noise exposures to determine if brainstem or midbrain auditory nuclei would be sufficient to support habituation to this specific stressor, as measured during an additional and drug-free loud noise exposure test. Our results indicate that auditory thalamic inactivation by muscimol disrupts acute HPA axis response specifically to loud noise. Importantly, habituation to repeated loud noise exposures was also prevented by reversible auditory thalamic inactivation, suggesting that this form of plasticity is likely mediated at, or in targets of, the auditory thalamus.