Topic: neurite outgrowth

Activation of pro-degenerative protein SARM1 in response to diverse physical and disease-relevant injuries triggers programmed axon death. Original studies indicated substantially decreased levels of SARM1 were required for neuroprotection. However, we demonstrate that lowering SARM1 levels by 50% in Sarm1 haploinsufficient mice delays axon degeneration in vivo (after sciatic nerve transection), in vitro (in response to diverse traumatic, neurotoxic, and genetic triggers), and partially prevents neurite outgrowth defects in mice lacking pro-survival factor NMNAT2. We also demonstrate the capa

The emergence of spontaneous activity in the form of synchronized bursting events (SBE) is considered to play a crucial role in activity-dependent development of neuronal networks. As inhibition matures, the spatiotemporal structure of activity becomes increasingly influenced by the balance between excitation and inhibition (E/I). Moreover, intricate interactions between excitatory (ENs) and inhibitory (INs) neurons may arise during their activity-dependent structural differentiation. However, how the resulting spatial embedding of INs and ENs in a network impacts on the spatiotemporal structu

Activity-dependent structural plasticity plays a pivotal role in the self-organization of neuronal networks. Emerging activity continuously feeds back into the growth process, regulating connectivity and activity homeostatically towards an optimal functional dynamic range. Transferred into cell culture, neurons follow the same homeostatic principles. They migrate and regrow neurites to establish synaptic connectivity and spontaneous network activity. Despite of homeostatic regulation, the resulting network structure and activity dynamics exhibit considerable variability across and within studi