The long-term behavioral deficits observed in depression are associated with altered spine synapses in specific neuronal circuits. A new study shows that chromatin remodeling decreases the expression of Ras-related C2 botulinum toxin substrate 1 (Rac1) and that the deficit in this small Rho GTPase is sufficient and necessary for altered spines and behavioral abnormalities in mice after social defeat (pages 337-344).
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