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Optogenetic Stimulation Reduces Neuronal Nitric Oxide Synthase Expression After Stroke.
Pendharkar, Arjun V; Smerin, Daniel; Gonzalez, Lorenzo; Wang, Eric H; Levy, Sabrina; Wang, Stephanie; Ishizaka, Shunsuke; Ito, Masaki; Uchino, Haruto; Chiang, Terrance; Cheng, Michelle Y; Steinberg, Gary K.
Afiliación
  • Pendharkar AV; Department of Neurosurgery and Stanford Stroke Center, Stanford University School of Medicine, Stanford, CA, USA.
  • Smerin D; Department of Neurosurgery and Stanford Stroke Center, Stanford University School of Medicine, Stanford, CA, USA.
  • Gonzalez L; Department of Neurosurgery and Stanford Stroke Center, Stanford University School of Medicine, Stanford, CA, USA.
  • Wang EH; Department of Neurosurgery and Stanford Stroke Center, Stanford University School of Medicine, Stanford, CA, USA.
  • Levy S; Department of Neurosurgery and Stanford Stroke Center, Stanford University School of Medicine, Stanford, CA, USA.
  • Wang S; Department of Neurosurgery and Stanford Stroke Center, Stanford University School of Medicine, Stanford, CA, USA.
  • Ishizaka S; Department of Neurosurgery and Stanford Stroke Center, Stanford University School of Medicine, Stanford, CA, USA.
  • Ito M; Department of Neurosurgery and Stanford Stroke Center, Stanford University School of Medicine, Stanford, CA, USA.
  • Uchino H; Department of Neurosurgery and Stanford Stroke Center, Stanford University School of Medicine, Stanford, CA, USA.
  • Chiang T; Department of Neurosurgery and Stanford Stroke Center, Stanford University School of Medicine, Stanford, CA, USA.
  • Cheng MY; Department of Neurosurgery and Stanford Stroke Center, Stanford University School of Medicine, Stanford, CA, USA. mycheng@stanford.edu.
  • Steinberg GK; Department of Neurosurgery and Stanford Stroke Center, Stanford University School of Medicine, Stanford, CA, USA. gsteinberg@stanford.edu.
Transl Stroke Res ; 12(2): 347-356, 2021 04.
Article en En | MEDLINE | ID: mdl-32661768
Post-stroke optogenetic stimulation has been shown to enhance neurovascular coupling and functional recovery. Neuronal nitric oxide synthase (nNOS) has been implicated as a key regulator of the neurovascular response in acute stroke; however, its role in subacute recovery remains unclear. We investigated the expression of nNOS in stroke mice undergoing optogenetic stimulation of the contralesional lateral cerebellar nucleus (cLCN). We also examined the effects of nNOS inhibition on functional recovery using a pharmacological inhibitor targeting nNOS. Optogenetically stimulated stroke mice demonstrated significant improvement on the horizontal rotating beam task at post-stroke days 10 and 14. nNOS mRNA and protein expression was significantly and selectively decreased in the contralesional primary motor cortex (cM1) of cLCN-stimulated mice. The nNOS expression in cM1 was negatively correlated with improved recovery. nNOS inhibitor (ARL 17477)-treated stroke mice exhibited a significant functional improvement in speed at post-stroke day 10, when compared to stroke mice receiving vehicle (saline) only. Our results show that optogenetic stimulation of cLCN and systemic nNOS inhibition both produce functional benefits after stroke, and suggest that nNOS may play a maladaptive role in post-stroke recovery.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Accidente Cerebrovascular / Optogenética Límite: Animals Idioma: En Revista: Transl Stroke Res Año: 2021 Tipo del documento: Article País de afiliación: Estados Unidos Pais de publicación: Estados Unidos
Texto completo
Añadir a Mi BVS
Imprimir
XML
PubMed Links
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Accidente Cerebrovascular / Optogenética Límite: Animals Idioma: En Revista: Transl Stroke Res Año: 2021 Tipo del documento: Article País de afiliación: Estados Unidos Pais de publicación: Estados Unidos