Vulnerability of hearing loss over age subsequent to the deletion of BDNF or CaV1.2 in the Cochlea

Resumen del póster presentado al 37th MidWinter Meeting of the Association for Research in Otorhinolaryngology celebrado en San Diego (US) del 22 al 26 de febrero de 2014.-- et al.
[Background]: We recently showed that tissue-specific deletion of brain-derived neurotrophic factor (BDNF) in the cochlea prevents loss of thresholds and auditory brainstem response (ABR), and loss of inner hair cell (IHC) synaptic ribbons after exposure to traumatizing sound (Zuccotti et al., 2012; Journal of Neuroscience, 32, 25, 8545-53). These effects could be partly mimicked by the deletion of L-type voltage-gated calcium channel CaV1.2 in the cochlea (Zuccotti et al., 2013; Frontiers in molecular neuroscience, 6). The present study aimed to assess if deletion of BDNF or CaV1.2 in the cochlea alters the vulnerability of hearing over age. [Methods]: We compared the hearing function by auditory brainstem response (ABR) and distortion product otoacoustic emission (DPOAE) measurements on young and aged (1) conditional BDNFPax2 KO mice (Zuccotti et al., 2012) with the deletion of BDNF in the whole cochlea, the dorsal cochlear nucleus, and inferior colliculus, and (2) conditional CaV1.2Pax2 KO mice (Zuccotti et al., 2013) with deletion CaV1.2 in the same tissues as in the BDNFPax2 KO mice. We furthermore analyzed the influence of acoustic noise exposure on hearing loss.
[Results]: Hearing function of both young and aged BDNFPax2KO and CaV1.2Pax2 KO mice were compared and related to outer hair cell (OHC) function and IHC synaptic structures. Suprathreshold ABR was analyzed in relation to young and aged mice. An interesting differential role of BDNF and CaV1.2 in the cochlea related to hair cell synaptic formation for sound processing became evident. [Conclusion]: We discuss the results in the context of a differential role of BDNF and CaV1.2 for hair cell and neuronal vulnerability during aging.