Drosophila NF-κB homologue “dorsal” is required for establishment of dorso-ventral polarity in the developing embryo (7). In the developing rat nervous system, levels of NF-κB activity change, with levels peaking in the cerebellum during the early postnatal period at a time when synaptogenesis is occurring (8). The particular NF-κB subunits expressed in neurons are also developmentally regulated; for example, inducible p50 homodimers and p65/cRel dimers are present in brains of young rats, but not in adults (9). A peptide inhibitor of NF-κB (SN50) blocks the ability of NGF to prevent death of cultured sympathetic neurons (10), suggesting a role for NF-κB in the control of neuronal death during development of the nervous system. The antiapoptotic role of NF-κB in developing neurons is seen in the mechanism whereby the protein synthesis inhibitor cycloheximide prevents neuronal apoptosis. Levels of cycloheximide that cause only a small impairment of protein synthesis can prevent apoptosis by inducing Bcl-2 and the antioxidant enzyme Mn-SOD (11), a process that depends on NF-κB activation; treatment of neurons with κB decoy DNA abolishes the antiapoptotic effect of cycloheximide. The presence of NF-κB in synaptic terminals located at considerable distances from the neuronal cell body, and its ability to be activated locally at those sites, strongly suggest that this transcription factor modulates synaptic function (2). Stimulation of glutamate receptors and membrane depolarization stimulate NF-κB activation in neurons, probably via a calcium-mediated mechanism. NF-κB is also activated in association with long-term potentiation (LTP) of synaptic trans-