Brain activity levels are tightly regulated to minimize imbalances in activity state. Deviations from the normal range of activity are deleterious and often associated with neurological disorders. To maintain optimal levels of activity, regulatory mechanisms termed homeostatic synaptic plasticity establish desired 'set points' for neural activity, monitor the network for deviations from the set point and initiate compensatory responses to return activity to the appropriate level that permits physiological function [1,2]. We speculate that impaired homeostatic control may contribute to the etiology of various neurological disorders including epilepsy and Alzheimer's disease, two disorders that exhibit hyperexcitability as a key feature during pathogenesis. Here, we will focus on recent progress in developing homeostatic regulation of neural activity as a therapeutic tool.
Keywords: Alzheimer's disease; CA3; Plk2; antiseizure drugs; dentate gyrus; epilepsy; homeostatic synaptic plasticity; kappa opioid receptors; mossy fiber; synaptoporin.