Neurodegeneration is a devastating sequel common to many neuropathological conditions. A current view is that the brain reacts to pathological insults by activating developmental programs for survival, regeneration and replacement of damaged neurons. For instance, after injury caused by e.g. acute brain trauma, the intracellular chloride homeostasis of mature central neurons becomes similar to immature neurons. As GABAA and Glycine receptors are functionally dependent on the transmembrane chloride electrochemical gradient the response to GABA and glycine is shifted from hyperpolarizing to depolarizing. So far, it has not been clear whether these posttraumatic changes are beneficial or detrimental. Recent evidence indicates that blocking of post-traumatic GABAA depolarization is neuroprotective. This mechanism involves a close interplay with the posttraumatic functional requirement of neurotrophic factors. In this meeting we will discuss these novel findings with the aim to construct a working hypothesis for future studies.