We studied the projections of the medial IC, which includes the FAK inhibitor classical central nucleus (CNIC) and the dorsal cortex (DCIC), and those of the lateral IC, equivalent to the classical external cortex (ECIC). Following unilateral injections of PHA-L into the medial IC, numerous terminal fibers are labeled bilaterally in the TLC. The ipsilateral projection is denser and targets the entire nucleus, whereas the contralateral projection targets significantly only the caudal half or two-thirds of the TLC. Fibers from the medial IC reach the TLC by two routes: as collaterals of

axons that travel in the commissure of selleckchem the IC and as collaterals of thick ipsilateral colliculogeniculate axons; the latter travel through the deep superior

colliculus on their way to the TLC. Within the TLC, individual IC fibers tend to run longitudinally. The injection of PHA-L into the lateral IC indicates that this subdivision sends a weak, bilateral projection to the TLC whose trajectory, morphology and distribution are similar to those of the projection from the medial IC. These results demonstrate that all subdivisions of the IC send projections to the TLC, suggesting that the IC may be one of the main sources of auditory input to this tectal nucleus. (C) 2010 IBRO. Published by Elsevier Ltd.

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“This study evaluated the protective role of p38 mitogen-activated protein kinase (p38 MAPK) inhibitors and sequestosome 1 (Sqstm1/A170/p62), a stress-induced signal modulator, in acoustic injury of the cochlea in mice. Erastin in vivo Two weeks after the exposure of mice to acoustic stress, threshold shifts of the auditory brainstem response (ABR) from the pre-exposure level and hair cell loss were evaluated. The activation of p38 MAPK was observed in cochlea by immunostaining 4 h after acoustic stress. To examine the role of p38 MAPK in tissue injury, its inhibitors were i.p. injected into male wild-type C57BL mice before the acoustic overexposure. The inhibitors SB202190 and SB203580 but not the inactive analogue SB202474 dose-dependently decreased the auditory threshold shift and outer hair cell loss induced by acoustic overexposure, suggesting the involvement of p38 MAPK in ototoxicity. We found that acoustic overexposure induced the up-regulation of Sqstm1 mRNA expression in the cochlea of wild-type mice and that SQSTM1-deficient mice exhibited an enhanced ABR threshold shift and hair cell loss, suggesting a role of SQSTM1 in the protection of tissue from acoustic stress.(C) 2010 IBRO. Published by Elsevier Ltd. All rights reserved.