Optogenetic Stimulation Increases Level of Antiapoptotic Protein Bcl-xL in Neurons

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D. A. Lanshakov¹, U. S. Drozd², and N. N. Dygalo^1,2*

¹Institute of Cytology and Genetics, Siberian Division of the Russian Academy of Sciences, 630090 Novosibirsk, Russia

²Novosibirsk National Research State University, 630090 Novosibirsk, Russia; E-mail: dygalo@bionet.nsc.ru

^* To whom correspondence should be addressed.

Received September 9, 2016

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The antiapoptotic protein Bcl-xL is associated with several neuroplastic processes such as formation of synapses, regulation of spontaneous and evoked synaptic responses, and release of neurotransmitters. Dependence of expression on activity of neurons is characteristic for many proteins participating in regulation of neuroplasticity. Whether such property is exhibited by the Bcl-xL protein was analyzed using in vivo optogenetic stimulation of hippocampal glutamatergic neurons expressing channelrhodopsin ChR2H134 under CAMKIIa promoter in the adeno-associated viral vector, followed by immunohistochemical determination of the level of Bcl-xL protein in these neurons and surrounding cells. Increase in the level of early response c-Fos protein following illumination with blue light was indicative of activation of these hippocampal neurons. The optogenetic activation of hippocampus resulted in a significant increase in the level of antiapoptotic protein Bcl-xL in the photosensitive neurons as well as in the surrounding cells. The dependence of the level of expression of Bcl-xL protein on the activity of neurons indicates that this protein possesses one more important property that is essential for participation in neuroplastic processes in the brain.

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KEY WORDS: protein Bcl-xL, protein c-Fos, AAV vector, optogenetics, hippocampal glutamatergic neuron, activity-dependent protein expression

DOI: 10.1134/S0006297917030129

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