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Isolation of Cortical Microglia with Preserved Immunophenotype and Functionality From Murine Neonates
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Published on: January 30, 2014

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Activation of microglia by histamine and substance P

Jin Zhu1, Chen Qu, Xiang Lu

  • 1Clinical Research Center, the First Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu, P. R. China.

Cellular Physiology and Biochemistry : International Journal of Experimental Cellular Physiology, Biochemistry, and Pharmacology
|August 30, 2014
PubMed
Abstract

Insights

Neuromediators like histamine and substance P activate microglia, leading to inflammation in the brain. This study identifies key receptors involved in this process.

Area of Science:

  • Neuroimmunology
  • Neuroinflammation

Background:

  • Microglia are key immune cells in the central nervous system (CNS).
  • Regulators of microglial activation are not fully understood.
  • Histamine and substance P are neuromediators with potential roles in microglial function.

Purpose of the Study:

  • To investigate the effect of histamine and substance P on microglial activation.
  • To identify the receptors mediating these effects.

Main Methods:

  • Primary microglia cultures were used to examine activation.
  • Confocal microscopy captured fluorescent images.
  • ELISA measured TNF-α and IL-6 levels.
  • Reactive oxygen species (ROS) and mitochondrial membrane potential were assessed.

Main Results:

  • Histamine and substance P induced microglial activation, producing ROS, TNF-α, and IL-6.
  • Receptor antagonists partially blocked these effects, implicating histamine receptors (H1, H4) and substance P receptors (NK-1, NK-2, NK-3).
  • Histamine caused mitochondrial membrane depolarization.

Conclusions:

  • Histamine and substance P activate microglia.
  • This activation leads to the release of pro-inflammatory factors.
  • These neuromediators contribute to microglia-mediated brain inflammation.

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