Neuroprotective Effect of σ1-Receptors on the Cell Model of Huntington’s Disease


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Abstract

Huntington’s disease is a hereditary neurodegenerative disease that primarily affects striatal neurons. Recent studies demonstrated abnormalities in calcium regulation in striatal neurons in Huntington’s disease, which leads to elimination of synaptic connections between cortical and striatal neurons. In the present study, we focused on the neuroprotective properties of σ1-receptor, because one of its main functions is associated with modulation of calcium homeostasis in cells. The application of selective σ1-receptor agonists to the corticostriatal cell culture restores synaptic connections between the cortical and striatal neurons. Based on the obtained data, we assume that σ1-receptor is a promising target for the development of drugs for the therapy of Huntington’s disease.

About the authors

A. V. Bol’shakova

Laboratory of Molecular Neurodegeneration, Peter the Great St. Petersburg State Polytechnic University

Email: mnlabspb@gmail.com
Russian Federation, St. Petersburg

N. A. Kraskovskaya

Laboratory of Molecular Neurodegeneration, Peter the Great St. Petersburg State Polytechnic University

Author for correspondence.
Email: ninakraskovskaya@gmail.com
Russian Federation, St. Petersburg

A. N. Gainullina

Laboratory of Molecular Neurodegeneration, Peter the Great St. Petersburg State Polytechnic University

Email: mnlabspb@gmail.com
Russian Federation, St. Petersburg

E. O. Kukanova

Laboratory of Molecular Neurodegeneration, Peter the Great St. Petersburg State Polytechnic University

Email: mnlabspb@gmail.com
Russian Federation, St. Petersburg

O. L. Vlasova

Laboratory of Molecular Neurodegeneration, Peter the Great St. Petersburg State Polytechnic University

Email: mnlabspb@gmail.com
Russian Federation, St. Petersburg

I. B. Bezprozvanny

Laboratory of Molecular Neurodegeneration, Peter the Great St. Petersburg State Polytechnic University; Department of Physiology, UT Southwestern Medical Center at Dallas

Author for correspondence.
Email: mnlabspb@gmail.com
Russian Federation, St. Petersburg; Dallas


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