Optogenetic modulation in stroke recovery.
Neurosurg Focus
; 40(5): E6, 2016 May.
Article
en En
| MEDLINE
| ID: mdl-27132527
ABSTRACT
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.
Palabras clave
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 linederived 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
Texto completo:
1
Colección:
01-internacional
Banco de datos:
MEDLINE
Asunto principal:
Recuperación de la Función
/
Accidente Cerebrovascular
/
Investigación Biomédica Traslacional
/
Optogenética
Límite:
Animals
/
Humans
Idioma:
En
Revista:
Neurosurg Focus
Asunto de la revista:
NEUROCIRURGIA
Año:
2016
Tipo del documento:
Article