This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. We will continue investigating the intercellular and intracellular signaling pathways that lead to neuronal death (or survival) following the elimination of excitatory synaptic input to the mammalian cochlear nucleus. A major initiative during the current grant period has been to use modern genetic analysis methods to begin assessing the biological mechanisms underlying differential responses of neonatal and adult animals to afferent deprivation (a critical period) of the mouse cochlear nucleus. Gene microarray technology was used to screen for genes that are differentially constitutively expressed in the cochlear nucleus during periods of differing susceptibility to peripheral deprivation and genes that are differentially regulated during vs. after this critical period in the first 48 hrs following peripheral deprivation (Harris et al., 2005;2006;2008). One of the most fascinating and important findings of these studies was that there is an enormous change in transcription during the transition between afferent dependent neuron survival (P2-P11;P=postnatal day) and afferent independent survival (>P14), which corresponds closely with the onset of hearing. But, there is essentially no significant change in mRNA expression between P14 and P21, the major period of hearing maturation.