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

  • Translated from Kletochnye Tekhnologii v Biologii i Meditsine (Cell Technologies in Biology and Medicine)
  • Published:
Bulletin of Experimental Biology and Medicine Aims and scope

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.

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Authors and Affiliations

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

    A. V. Bol’shakova, N. A. Kraskovskaya, A. N. Gainullina, E. O. Kukanova, O. L. Vlasova & I. B. Bezprozvanny

  2. Department of Physiology, UT Southwestern Medical Center at Dallas, Dallas, USA

    I. B. Bezprozvanny

Authors
  1. A. V. Bol’shakova
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  2. N. A. Kraskovskaya
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  3. A. N. Gainullina
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  4. E. O. Kukanova
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  5. O. L. Vlasova
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  6. I. B. Bezprozvanny
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Corresponding authors

Correspondence to N. A. Kraskovskaya or I. B. Bezprozvanny.

Additional information

Translated from Kletochnye Tekhnologii v Biologii i Meditsine, No. 3, pp. 160-167, July, 2017

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Bol’shakova, A.V., Kraskovskaya, N.A., Gainullina, A.N. et al. Neuroprotective Effect of σ1-Receptors on the Cell Model of Huntington’s Disease. Bull Exp Biol Med 164, 252–258 (2017). https://doi.org/10.1007/s10517-017-3968-7

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  • DOI: https://doi.org/10.1007/s10517-017-3968-7

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