Serotonin differentially modulates the functional properties of damaged and intact motoneurons of the frog spinal cord

Cover Page

Abstract


The role of serotonin in the recovery of motor functions in spinal cord injuries is intensively studied, but the mechanism of its action remains unclear. In this work, we used the preparation of an isolated segment of the spinal cord of an adult frog to compare the electrophysiological properties of damaged and intact lumbar moto- neurons and the modulating effect of serotonin (5-HT) on them. Due to specific morphology of the motoneurons (a very branched dendritic tree), we could reliably obtain damaged (on the surface of the slice) and intact moto- neurons (in the depth of the slice). Using intracellular recording, we found significant differences between these groups of neurons in the resting membrane potential, input resistance, properties of the action potential (amplitude, duration, fast and medium phases of the afterhyperpolarization), the frequency of spikes. We found that 5-HT reduced the amplitude of the afterhyperpolarization and increased the frequency of spikes in intact neurons, whereas in damaged motoneurons, 5-HT increased the amplitude of the afterhyperpolarization and did not affect the frequency of discharges. The results of the study show that the properties of the motoneurons and the effect of neuromodulators on them, in particular, 5-HT, can change after damage.


N. I. Kalinina

Институт эволюционной физиологии и биохимии им. И.М. Сеченова Российской Академии наук

Author for correspondence.
Email: nkalinina54@mail.ru

Russian Federation, Санкт-Петербург

A. V. Zaitsev

Институт эволюционной физиологии и биохимии им. И.М. Сеченова Российской Академии наук; Санкт-Петербургский государственный университет

Email: aleksey_zaitsev@mail.ru

Russian Federation, Санкт-Петербург

N. P. Vesselkin

Институт эволюционной физиологии и биохимии им. И.М. Сеченова Российской Академии наук; Санкт-Петербургский государственный университет

Email: aleksey_zaitsev@mail.ru

Russian Federation, Санкт-Петербург

  1. Schmidt B.J., Jordan L.M. // Brain Res. Bull. 2000. V. 53. № 5. P. 689–710.
  2. Murray K.C., Stephens M.J., Ballou E.W., et al. // J. Neurophysiol. 2011. V. 105. P. 731–748.
  3. Alvarez F.J, Pearson J.C., Harrington D., et al. // J. Comp. Neurol. 1998. V. 393. P. 69–83.
  4. Xia Y., Chen D., Xia H., et al. // Neurosci. Lett. 2017. V. 649. P. 70–77.
  5. Davies M.L., Kirov S.A., Andrew R.D. // J. Neurosci. Methods. 2007. V. 166. P. 203–216.
  6. Carp J.S., Tennissen A.M., Mongeluzi D.L., et al. // J. Neurophysiol. 2008. V. 100. P. 474–481.
  7. Kalinina N.I., Kurchavyi G.G., Zaitsev A.V., Vessel- kin N.P. // J. Evolut. Biochem. Physiol. 2016. V. 52. № 5. Р. 359–368.
  8. Kalinina N.I., Zaitsev A.V., Vesselkin N.P. // J. Comp. Physiol. A. 2018. V. 204. № 3. P. 329–337.
  9. Dityatev A.E., Chmykhova N.M., Dityateva G.V., et al. // J. Comp. Neurol. 2001. V. 430. P. 433–447.
  10. Diaz-Rios M., Dombeck D.A., Webb W.W., Harris- Warrick R.M. // J. Neurophysiol. 2007. V. 98. P. 2157– 2167.
  11. Hsiao C.F., Trueblood P.R., Levine M.S., Chan- dler S.H. // J. Neurophysiol. 1997. V. 77. P. 2910– 2924.
  12. Miles G.B., Sillar K.T. // Physiology. 2011. V. 26. P. 393–441.
  13. Perrier J-F., Rasmussen H.B., Christensen R.K., Pe- tersen A.V. // Curr. Pharm. Des. 2013. V. 19. № 24. P. 4371–4384.
  14. Sah P. // TINS. 1996. V. 19. № 4. P. 150–154.

Views

Abstract - 24

PDF (Russian) - 26

PlumX


Copyright (c) 2019 Российская академия наук