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Forskolin As a Neuroprotector and Modulator of Glutamate-Evoked Ca2+ Entry into Cerebellar Neurons

  • M. A. Ivanova
  • L. S. Sitnikova
  • Yu. D. Stepanenko
  • T. V. Karelina
  • D. A. Sibarov
  • P. A. AbushikEmail author
  • S. M. Antonov
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Abstract

The analysis of neuronal viability of cerebellar neurons in primary culture during long-lasting (240 min) treatment with glutamate revealed that forskolin (1 μM), an adenylate cyclase activator, prevents apoptosis and necrosis of cells, thus exhibiting neuroprotective properties. As the cytotoxic action of glutamate causes an increase of the intracellular Ca2+ concentration, we further studied forskolin influence on glutamate-evoked Ca2+ responses of neurons. A short-time pretreatment with 1 μM forskolin significantly decreases Ca2+ entry into neurons during glutamate action. The obtained results demonstrate an important role of adenylate cyclase and cAMP in regulation of the Ca2+ entry into neurons and intracellular signaling pathways preventing neuronal death of cerebellar neurons in excytotoxic stress.

Keywords:

neurodegeneration glutamate forskolin neuroprotection apoptosis calcium 

Notes

ACKNOWLEDGMENTS

The work was supported by the Russian Foundation for Basic Research (project no. 16-04-00653) and by the scholarship of the Russian Federation President. Sopported by RF state program № АААА-А18-118012290427-7.

COMPLIANCE WITH ETHICAL STANDARDS

Conflict of interests. The authors declare that they have no conflict of interest.

Statement on the welfare of animals. This article does not contain any studies involving animals performed by any of the authors.

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Copyright information

© Pleiades Publishing, Ltd. 2018

Authors and Affiliations

  • M. A. Ivanova
    • 1
  • L. S. Sitnikova
    • 1
  • Yu. D. Stepanenko
    • 1
  • T. V. Karelina
    • 1
  • D. A. Sibarov
    • 1
  • P. A. Abushik
    • 1
    Email author
  • S. M. Antonov
    • 1
  1. 1.Sechenov Institute of Evolutionary Physiology and Biochemistry, Russian Academy of SciencesSt. PetersburgRussia

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