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Minocycline does not affect long-term potentiation in the anterior cingulate cortex of normal adult mice

Qian Song1, Ming-Gang Liu2,3, Min Zhuo4,5

  • 1Center for Neuron and Disease, Frontier Institutes of Science and Technology, Xi'an Jiaotong University, Xi'an, 710049, China. sqyz3000@sina.com.

Molecular Pain
|May 3, 2015
PubMed

Insights

Minocycline, a microglial activation inhibitor, did not affect cortical plasticity in the anterior cingulate cortex (ACC). These findings indicate that neurons, not microglia, are the primary drivers of chronic pain-related cortical plasticity.

Area of Science:

  • Neuroscience
  • Pain Research
  • Cellular Biology

Background:

  • Activated microglia are implicated in spinal cord dorsal horn signaling in chronic pain.
  • The role of microglia in cortical plasticity related to chronic pain remains less understood.
  • Cortical plasticity in the anterior cingulate cortex (ACC) is recognized as crucial for chronic pain.

Purpose of the Study:

  • To investigate the role of microglia in cortical plasticity within the ACC.
  • To determine if inhibiting microglial activation affects synaptic plasticity in the ACC.

Main Methods:

  • Utilized a 64-channel multi-electrode array recording system in adult mice.
  • Administered minocycline, a microglial activation inhibitor, via bath application.
  • Induced and measured postsynaptic long-term potentiation (post-LTP) and presynaptic long-term potentiation (pre-LTP) in the ACC.

Main Results:

  • Minocycline did not alter post-LTP induced by theta burst stimulation in the ACC.
  • Minocycline did not affect pre-LTP induced by low-frequency stimulation combined with a GluK1-containing kainate receptor agonist.
  • The spatial distribution of both post-LTP and pre-LTP within the cingulate network remained unchanged after minocycline treatment.

Conclusions:

  • Minocycline does not influence cingulate plasticity.
  • Neurons are the principal mediators of pain-related cortical plasticity.
  • Microglia do not appear to play a significant role in ACC cortical plasticity relevant to chronic pain.

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