Blocking the glial function suppresses subcutaneous formalin-induced nociceptive behavior in the rat

Area of Science:

• Neuroscience
• Pain Research
• Cell Biology

Background:

• Orofacial nociception involves complex neural circuits.
• The role of glial cells, particularly astrocytes, in trigeminal pain processing remains incompletely understood.

Purpose of the Study:

• To investigate the necessity of glial cells in the trigeminal nucleus caudalis (Sp5C) for orofacial nociception.
• To elucidate the role of astrocyte-neuron communication in pain signaling.

Main Methods:

• Immunohistochemistry and immunoelectron microscopy were employed.
• Behavioral assessments were conducted following formalin injection.
• Pharmacological agents, carbenoxolone (CBX) and fluorocitrate (FCA), were used to inhibit gap junctions and glial metabolism, respectively.

Main Results:

• Inhibition of glial metabolism (FCA) and gap junction function (CBX) significantly reduced nociceptive behavior and scratching.
• FCA attenuated the expression of neuronal and astrocyte markers (Fos/NeuN and Fos/GFAP) in Sp5C.
• Immunoelectron microscopy revealed increased heterotypic gap junctions (HGJs) between astrocytes and neurons in Sp5C after formalin injection.

Conclusions:

• Astrocytes in Sp5C are crucial for orofacial nociception.
• Astrocyte-neuron heterotypic gap junctions (Cx32/Cx43 HGJs) are involved in regulating pain signaling in the trigeminal nucleus caudalis.