Abstract

The ATP-gated cation channel receptor P2X 3 is associated with nociceptive primary sensory neurons. We have, using immunohistochemistry, examined the expression of P2X 3 in rat trigeminal ganglia 4–22 days after ligation/section or chronic constriction of the mandibular inferior alveolar nerve. In the normal trigeminal ganglion the anti-P2X 3 receptor antibody labeled 37–58% of all neurons. Double labeling demonstrated that about 70–95% of the small neurons that bind the isolectin I-B4 displayed P2X 3-immunoreactivity, and that about 40% of larger RT97-positive nerve cells were P2X 3 receptor-immunoreactive. At 4 and 10 days after inferior alveolar nerve injury, the proportion of P2X 3-immunoreactive neurons had increased to about 65% (range 52–78%). Examinations at the injury sites showed an intense P2X 3 receptor-immunoreactivity in nerve endings. At longer survival stages the proportion of P2X 3 receptor-positive sensory neurons had returned to control values. These results show that the P2X 3 receptor is transiently upregulated and anterogradely transported in trigeminal primary sensory neurons after nerve injury. Since the receptor is accumulated in injured nerve endings, it may be associated with abnormal impulse propagation from these sites.

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