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Optogenetic Stimulation Reduces Neuronal Nitric Oxide Synthase Expression After Stroke.

Authors :
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.
Source :
Translational Stroke Research; Apr2021, Vol. 12 Issue 2, p347-356, 10p
Publication Year :
2021

Abstract

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. [ABSTRACT FROM AUTHOR]

Details

Language :
English
ISSN :
18684483
Volume :
12
Issue :
2
Database :
Complementary Index
Journal :
Translational Stroke Research
Publication Type :
Academic Journal
Accession number :
149025397
Full Text :
https://doi.org/10.1007/s12975-020-00831-y