Pituitary adenylate cyclase activating polypeptide (PACAP) is a regulatory and cytoprotective
neuropeptide, its deficiency implies accelerated aging in mice. It is present in the
auditory system having antiapoptotic effects. Expression of Ca2+-binding proteins
and its PAC1 receptor differs in the inner ear of PACAP-deficient (KO) and wild-type
(WT) mice. Our aim was to elucidate the functional role of PACAP in the auditory system.
Auditory brainstem response (ABR) tests found higher hearing thresholds in KO mice
at click and low frequency burst stimuli. Hearing impairment at higher frequencies
showed as reduced ABR wave amplitudes and latencies in KO animals. Increase in neuronal
activity, demonstrated by c-Fos immunolabeling, was lower in KO mice after noise exposure
in the ventral and dorsal cochlear nuclei. Noise induced neuronal activation was similar
in further relay nuclei of the auditory pathway of WT and KO mice. Based on the similar
inflammatory and angiogenic protein profile data from cochlear duct lysates, neither
inflammation nor disturbed angiogenesis, as potential pathological components in sensorineural
hearing losses, seem to be involved in the pathomechanism of the presented functional
and morphological changes in PACAP KO mice. The hearing impairment is probably concomitant
with the markedly accelerated aging processes in these animals.