Our in vitro data on neuronal survival can be associated with in vivo observations of the SG. The expression of BDNF in the cochlea generally seems to vary during the period under study. At birth, BDNF is observed in rat inner and outer hair cells and along the length of the cochlea and exists in the supporting cells of the mouse organ of Corti Lenalidomide TNF-alpha Receptor inhibitor only in the apical turn. Wheeler et al. and Wiechers et al. Described that BDNF mRNA in HCs dropped to background levels by P3 P4. Wiechers et al. Discovered BDNF mRNA in SCs and outside HCs at P6 P8, while Ylikoski et al. Observed BDNF mRNA in both internal HCs and external HCs at P7. Weichers et al. evaluated the expression of BDNF in the protein level during the first two post-natal weeks in mice, using immunohistochemistry. They discovered that BDNF occurs in internal HCs and outer HCs at P1, and then disappears at P3. Nevertheless, at P3 BDNF is situated in some SG neurons. BDNF then reappears in SCs and HCs Metastatic carcinoma at P6, and is observed at high levels in SG nerves. At P10, BDNF is only present in some SCs and in scattered SG neurons. These results claim that HCs produce BDNF through the first few days after birth, with a decline around P3 P4, but recovery by P6 P7. SG nerves also transiently convey BDNF, start around P6. R?ttiger et al. showed that BDNF is not expressed in the organ of Corti, but in the SG in adult gerbils. An average decline in expression was noticed in turns during aging, while there was no change in BDNF expression in the apical turn. On the other hand, a current study by Liu et al. Precise individual cochlear individuals showed no expression of BDNF protein both in the organ of Corti or in the SG on person. Our data show that SG neurons and neurites are very sensitive and painful to BDNF during the time where declines in production are noticed, around P3 P5. This can be in keeping with electrophysiological experiments on P3 P8 neonatal mouse SG. Adamson et al. demonstrated that BDNF alters the endogenous membrane channel types and properties in such a way as to create faster housing and kinetics. It could be speculated that Akt and/or p38 signaling may give rise to these results. It’s possible that early postnatal production of BDNF within the organ of Corti keeps neurites and SG neurons during the period of reorganization of innervation. The decline in production might then produce apoptosis, with those neurons that fundamentally survive having effectively innervated HCs, while neurons that fail to synapse on HCs die from not enough trophic support. SG neurons are reported to bear large apoptosis throughout the first post-natal week in mice. Our signaling results suggest that a number of pathways participate in transmitting the effects of TrkB receptor activation to the nucleus. Our results are summarized in Fig. 6. The powerful effects of FTI 277 on number suggest a significant part for Ras in mediating the success and neuritogenesis promoting effects of BDNF.