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Related Experiment Video

Updated: Mar 22, 2026

Magnetic Isolation of Microglial Cells from Neonate Mouse for Primary Cell Cultures
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Methamphetamine alters microglial immune function through P2X7R signaling.

Nicole C Fernandes1, Uma Sriram1, Larisa Gofman1

  • 1Department of Pathology and Laboratory Medicine, Lewis Katz School of Medicine at Temple University, MERB 845A, 3500 N. Broad Street, Philadelphia, 19140, PA, USA.

Journal of Neuroinflammation
|April 28, 2016
PubMed
Summary

Methamphetamine (METH) increases the expression and membrane localization of the P2X7 receptor (P2X7R) in microglia. This P2X7R activation enhances microglial migration and phagocytosis, suggesting P2X7R antagonists as potential therapeutics for neuroinflammation.

Keywords:
MethamphetamineMicrogliaPurinergic receptor X7

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Area of Science:

  • Neuroscience
  • Immunology
  • Pharmacology

Background:

  • Purinoceptors, particularly the ionotropic P2X7 receptor (P2X7R), are implicated in chronic inflammation and neurodegeneration.
  • P2X7R modulates neuroinflammatory signaling and microglial activation, suggesting a key role in neuroinflammatory conditions.

Purpose of the Study:

  • To investigate the effects of methamphetamine (METH) on microglial P2X7R expression and function.
  • To explore the role of P2X7R in METH-induced microglial activation.

Main Methods:

  • Primary rat microglial cells (ESdMs) were treated with METH to assess P2X7R gene and protein expression (Taqman PCR, Western blot).
  • Microglial migration and phagocytosis assays were performed, with and without P2X7R antagonist treatment or siRNA silencing.
  • In vivo studies utilized an escalating METH dose mouse model to examine P2X7R and tyrosine hydroxylase (TH) expression via immunohistochemistry.

Main Results:

  • METH significantly increased P2X7R mRNA and protein expression in ESdMs, with enhanced membrane localization.
  • METH treatment promoted microglial migration and phagocytosis in a P2X7R-dependent manner.
  • Silencing P2X7R reduced METH-induced pro-inflammatory cytokine production (TNF-α, IL-10).
  • In vivo, METH exposure increased P2X7R and decreased TH expression in mouse striata.

Conclusions:

  • P2X7R plays a significant role in regulating microglial activation and effector functions in response to METH.
  • Targeting P2X7R with antagonists may offer a therapeutic strategy for neuroinflammatory disorders associated with substance abuse.