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Coexpression of Nav1.8 and VGLUTs in the Rat Trigeminal Ganglion and Tooth Pulp

  • Anatomy & Biological Anthropology
  • Abbr : Anat Biol Anthropol
  • 2026, 39(3), pp.259~268
  • DOI : 10.11637/aba.2026.39.3.259
  • Publisher : 대한체질인류학회
  • Research Area : Medicine and Pharmacy > Anatomy
  • Received : August 13, 2026
  • Accepted : September 27, 2026
  • Published : June 30, 2026

김윤경 1,  박숙경 1,  배진영 1,  Sang Kyoo Paik 1,  Kim Yun Sook ORD ID 1,  BAE YONG-CHUL ORD ID 1

1경북대학교 치과대학 구강해부학교실

Accredited

ABSTRACT

Voltage-gated sodium channel 1.8 (Nav1.8) is important for the generation and propagation of action potentials in primary nociceptors. Nav1.8 is also involved in acute pain and inflammation-induced pain hypersensitivity. However, it remains unclear whether Nav1.8-mediated nociceptive input is associated with distinct vesicular glutamate transporters (VGLUTs). To investigate this, we examined the coexpression of Nav1.8 with VGLUT1 or VGLUT2 in the rat trigeminal ganglion (TG) and tooth pulp using fluorescence immunohistochemistry. Most Nav1.8-immunopositive (Nav1.8 + ) neurons in the TG and Nav1.8 + nerve fibers in the tooth pulp coexpressed VGLUT2, whereas coexpression with VGLUT1 was very rare. In addition, Nav1.8 + neurons in the TG coexpressed substance P, calcitonin gene-related peptide, or isolectin B4, which are markers of nociceptive neurons, but rarely coexpressed parvalbumin or neurofilament 200, which are expressed in relatively large-diameter sensory neurons. Our findings suggest that Nav1.8 is mostly expressed in nociceptive neurons in the TG and nerve fibers in the tooth pulp and is preferentially associated with VGLUT2 rather than VGLUT1. The selective coexpression of Nav1.8 and VGLUT2 suggests that Nav1.8 + nociceptors may contribute to nociceptive transmission through VGLUT2-dependent glutamatergic neurotransmission.

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