Expression profiles of TACAN in the muscle of a rat model of delayed onset muscle soreness

Abstract

Delayed onset muscle soreness (DOMS) is defined as pain or mechanical hyperalgesia induced after unaccustomed strenuous muscular work, including lengthening contractions (LC), yet the molecular mechanism is largely unknown. Recently, TACAN (also referred to as Tmem120a) has been reported as an ion channel involved in sensing mecha­nical pain (Beaulieu–Laroche et al., Cell, 2020) and mechanical hyperalgesia after inflammation in the skin (Bonet et al., J Pain, 2020). However, the role of TACAN in DOMS is unknown. Here we examined the expression profiles of TACAN mRNA in the muscle using a rat model of DOMS. Under isoflurane anesthesia, male Sprague–Dawley rats (aged 9–12 weeks, weighing 295–397 g) were exposed to repetitive LC of the lower leg extensor muscles [mainly tibialis anterior (TA) muscle]. Shallow and deep layers of the TA were sampled 24 h after LC, when mechanical hyperalgesia reaches at its peak after LC (Hayashi et al., Eur J Pain, 2017). The expression level of TACAN and nerve growth factor (NGF) mRNA was measured using real–time RT–PCR. In the shallow layer of the TA, the TACAN and NGF mRNA level were significantly increased on the ipsilateral side of LC, compared to the contralateral side. In the deep layer of the TA, the expression level was unchanged. These results suggest that TACAN upregulated in the shallow layer of the muscle that underwent LC is involved in the generation of mechanical hyperalgesia in DOMS.