gms | German Medical Science

Acoustic trauma often resultsin damaged cochlear, reorganized tonotopic map,altered firing activates and synaptic connections imbalance between excitation and inhibition was thought account for elevated excitability of central auditory nuclei, forming perception of phantom sound in auditory cortex the case of tinnitus. GABAergic neurons in auditory cortex (AC) ramify profusely locally inhibit glutamatergic excitation, many neurological disorders were reported caused by impaired GABAergic neurons. Parvalbumin (PV) contain neurons was largest population among inhibitory neurons, playing a critical role in shaping and synchronizing neuronal activitie.

We found 1 hour continuous unilateral noise exposed rat (16 kHz, 116 dB SPL) significantly caused increase of auditory brainstem evoked response threshold of exposed ear (left), while unexposed ear (right) remained unchanged,examined 7 days later. The number of PV neurons decreased significantly in affected contra-lateral auditory cortices (right AC) compar with those less affected ipsi-lateral auditory cortices (left AC). No difference was found for PV neurons density between left and right of control group. Substantially stronger staining intensity of PV protein was also observed in right AC of noise exposed animals, more abundant PV protein of affected AC region was confirmed with Western-blotting techniques. The reduced number was indicative of impaired function of GABAergic inhibition; however, more PV expression suggested that compensatory mechanism might be involved to correct compromised inhibition.

The finding provid evidence acoustic trauma induced hearing loss might lead to loss of cortical PV interneuron to reduce cortical inhibition,homeostasis mechanism enables surviving PV neurons more excitable to recover inhibitory level.

Unterstützt durch: Department of Otorhinolarngology head and neck surgery, Anhui Provincial Hospital Hefei, China

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