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Use of the Operant Orofacial Pain Assessment Device OPAD to Measure Changes in Nociceptive Behavior
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Gi protein functions in thalamic neurons to decrease orofacial nociceptive response.

Jennifer Strand1, Crystal Stinson2, Larry L Bellinger2

  • 1Department of Psychology, University of Texas at Arlington, Arlington, TX 76019, United States.

Brain Research
|May 16, 2018
PubMed
Summary

Inhibiting excitatory neurons in the ventroposterior thalamus (VP) reduced orofacial pain signals in rats. This pain reduction was partly mediated by G-protein-coupled inwardly-rectifying potassium channels (GIRKs).

Keywords:
GABAGlutamateNeuronsOrofacialPainVentral posterior medial thalamus

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Area of Science:

  • Neuroscience
  • Pain Research
  • Thalamic Function

Background:

  • Orofacial pain involves trigeminal pathways projecting through the thalamus.
  • The specific role of the ventroposterior thalamic complex (VP) in orofacial pain transmission remains unclear.

Purpose of the Study:

  • To investigate the role of VP neurons in orofacial pain processing.
  • To determine if inhibiting VP neuronal activity can modulate nociception.

Main Methods:

  • Utilized a designer receptor exclusively activated by a designer drug (DREADD) approach to inhibit VP cells in Sprague Dawley rats.
  • Administered formalin to the masseter muscle to induce orofacial nociception.
  • Recorded local field potentials (LFPs) and measured facial rubbing behavior.
  • Used tertiapin-Q to block G-protein-coupled inwardly-rectifying potassium channels (GIRKs).
  • Performed immunostaining for VGLUT2 and VGAT to identify cell types.

Main Results:

  • Formalin injection significantly increased LFPs and nociceptive responses.
  • Activation of inhibitory DREADDs in VP neurons significantly reduced LFPs and orofacial nociception.
  • Blocking GIRK channels with tertiapin-Q reversed the inhibitory effects, increasing LFPs and nociception.
  • Immunostaining revealed that most DREADD-transfected cells were excitatory (VGLUT2+).

Conclusions:

  • Inhibition of excitatory VP neurons effectively reduces orofacial nociception and associated electrical activity.
  • The observed inhibitory effects are, in part, mediated by the activation of GIRK channels.
  • These findings highlight the VP as a critical node in orofacial pain pathways.