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The Effect of Neuronal Activity on Glial Thrombin Generation

Authors
  • Gera, Orna1, 2
  • Shavit-Stein, Efrat1
  • Chapman, Joab1, 2, 3, 4
  • 1 Tel HaShomer, Laboratory for Neurology Research Department of Neurology and the Joseph Sagol Neuroscience Center, Chaim Sheba Medical Center, Ramat Gan, Israel , Ramat Gan (Israel)
  • 2 Tel Aviv University, Department of Physical Therapy, Sackler Faculty of Medicine, Tel Aviv, Israel , Tel Aviv (Israel)
  • 3 Tel Aviv University, Department of Neurology, Sackler Faculty of Medicine, Tel Aviv, Israel , Tel Aviv (Israel)
  • 4 Tel Aviv University, Robert and Martha Harden Chair in Mental and Neurological Diseases, Sackler Faculty of Medicine, Tel Aviv, Israel , Tel Aviv (Israel)
Type
Published Article
Journal
Journal of Molecular Neuroscience
Publisher
Springer-Verlag
Publication Date
Jan 25, 2019
Volume
67
Issue
4
Pages
589–594
Identifiers
DOI: 10.1007/s12031-019-01265-4
Source
Springer Nature
Keywords
License
Yellow

Abstract

Thrombin through its receptor PAR-1 plays an important role in the peripheral nervous system. PAR-1 is located at the microvilli of Schwann cells at the node of Ranvier, and thrombin is generated by the coagulation system on these glial structures. In the present study, we examined the link between neuronal activity and modulation of thrombin generation by glial Schwann cells. Thrombin activity was assessed in sciatic nerves in reaction to high KCl as a model of neuronal activity. We demonstrated a significant transient effect of high KCL on thrombin activity (F(5, 20) = 42.65, p < 0.0001, by ANOVA) compared to normal KCl levels. Since the sciatic nerve includes components of axons and Schwann cell myelin sheath, we continued to investigate the effect of high KCl on a Schwannoma cell line as a model for nodal Schwann cell microvilli. We demonstrated a transient decrease in thrombin activity in response to high extracellular KCl (F(1, 18) = 9.56, p = 0.0063). The major neuronal inhibitor of thrombin is PN-1, and we therefore measured the effect of high KCL on PN-1 immunofluorescence intensity. We found significantly higher PN-1 staining intensity 3 min after the application of high KCL in comparison to cells exposed to high KCL for 7 min and to cells in regular KCL (F(2, 102) = 8.4737, p < 0.0004), and this effect may explain the changes in thrombin activity. The present results support an interaction between neuronal activity and the coagulation pathway as a novel mechanism for neuron-glia crosstalk at the node of Ranvier.

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