Galanin protects against nerve injury after shear stress in primary cultured rat cortical neurons

PLoS One. 2013 May 14;8(5):e63473. doi: 10.1371/journal.pone.0063473. Print 2013.

Abstract

The neuropeptide galanin and its receptors (GalR) are found to be up-regulated in brains suffering from nerve injury, but the specific role played by galanin remains unclear. This study aimed to explore the neuroprotective role of galanin after shear stress induced nerve injury in the primary cultured cortical neurons of rats. Our results demonstrated that no significant changes in cell death and viability were found after galanin treatment when subjected to a shear stress of 5 dyn/cm(2) for 12 h, after increasing magnitude of shear stress to 10 dyn/cm(2) for 12 h, cell death was significantly increased, while galanin can inhibit the nerve injury induced by shear stress with 10 dyn/cm(2) for 12 h. Moreover, Gal2-11 (an agonist of GalR2/3) could also effectively inhibit shear stress-induced nerve injury of primary cultured cortical neurons in rats. Although GalR2 is involved in the galanin protection mechanism, there was no GalR3 expression in this system. Moreover, galanin increased the excitatory postsynaptic currents (EPSCs), which can effectively inhibit the physiological effects of shear stress. Galanin was also found to inhibit the activation of p53 and Bax, and further reversed the down regulation of Bcl-2 induced by shear stress. Our results strongly demonstrated that galanin plays a neuroprotective role in injured cortical neurons of rats.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Apoptosis / drug effects
  • Cells, Cultured
  • Cerebral Cortex / pathology*
  • Cerebral Cortex / physiopathology
  • Cranial Nerve Injuries / metabolism
  • Cranial Nerve Injuries / pathology*
  • Cranial Nerve Injuries / physiopathology
  • Cranial Nerve Injuries / prevention & control*
  • Excitatory Postsynaptic Potentials / drug effects
  • Galanin / pharmacology*
  • Gene Expression Regulation / drug effects
  • Neurons / drug effects*
  • Neurons / pathology
  • Neuroprotective Agents / pharmacology*
  • Proto-Oncogene Proteins c-bcl-2 / metabolism
  • Rats
  • Receptors, Galanin / genetics
  • Shear Strength
  • Signal Transduction / drug effects
  • Stress, Mechanical*
  • Tumor Suppressor Protein p53 / metabolism
  • bcl-2-Associated X Protein / metabolism

Substances

  • Neuroprotective Agents
  • Proto-Oncogene Proteins c-bcl-2
  • Receptors, Galanin
  • Tumor Suppressor Protein p53
  • bcl-2-Associated X Protein
  • Galanin

Grants and funding

This project was supported by National Basic Research Program of China (973 Program, 2011CB710901, www.most.gov.cn), the National Natural Science Foundation of China (No.31100666, 11120101001, 10925208 www.nsfc.gov.cn). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.