Stroke is one of the leading contributors to morbidity, mortality, and health care costs in the United States. Although several preclinical strategies have shown promise in the laboratory, few have succeeded in the clinical setting. Optogenetics represents a promising molecular tool, which enables highly specific circuit-level neuromodulation. Here, the conceptual background and preclinical body of evidence for optogenetics are reviewed, and translational considerations in stroke recovery are discussed.
Keywords: ArchT = archaerhodopsin; BDNF = brain-derived neurotrophic factor; CAP-23 = cytoskeleton-associated protein 23; CNO = clozapine-N-oxide; DREADD; DREADD = designer receptor exclusively activated by designer drugs; EGF = epidermal growth factor; FGF-2 = basic fibroblast growth factor 2; GABA = γ-aminobutyric acid; GAP-43 = growth-associated protein 43; GDF10 = growth differentiation factor 10; GDNF = glial cell line–derived neurotrophic factor; IGF1 = insulin-like growth factor 1; MARCKS = myristoylated alanine-rich protein kinase C substrate; NGF = nerve growth factor; NTF3 = neurotrophin-3; WGA = wheat germ agglutinin; designer receptor exclusively activated by designer drugs; iM1 = ipsilesional primary motor cortex; ischemia; neuroregeneration; optogenetics; plasticity; stroke.