Aims: 

PACAP is a multifunctional neuropeptide with well known neuroprotective effects. The involvement of PACAP in sensory processing has also been documented. We have provided evidence that PACAP is neuroprotective in several models of retinal degeneration in vivo and protects cochlear cells against oxidative stress-induced apoptosis. The aim of the present study is the morphological examination of the retina and the inner ear of PACAP deficient mice to examine the effect of endogenous PACAP in sensory functions.

Methods: 

In the first part of the study we investigated the retinal structures of mice and we compared the degree of retinal damage in wild type and PACAP KO mice in ischemic retinal insult. Mice underwent 10 min of bilateral carotid artery occlusion followed by 2-week reperfusion period. In the second part of the study we examined the localization of Ca²⁺ buffering proteins (parvalbumin, calretinin, calbindin), which are essential for the normal hearing, and PAC1-receptors in the two groups.

Results: 

Histological analysis of normal retina did not show morphological difference between the two groups, but PACAP KO animals had greater retinal damage after ischemia compared to wild mice. We did not find morphological differences in the inner ear either, but with immunohistochemistry PACAP KO animals showed more pronounced Ca²⁺ buffering protein immunpositivity and less PAC1-receptor immunopositivity in the cochlear cells.

Conclusion: 

Elevated endolymphatic Ca²⁺ is deleterious for the cochlear function, against which the high cc. of Ca²⁺ buffers in hair cells may protect. Meanwhile, the greater retinal damage and the increased immunoreactivity of Ca²⁺ buffering proteins in the absence of PACAP provide further evidence for the important role of PACAP in the sensory processes.

Support: 

OTKA K72592, F67830, CNK78480, ETT278-04/2009, Bolyai Scholarship, Richter Foundation