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Papers of the Week

Papers: 11 Jun 2022 - 17 Jun 2022

Animal Studies

2022 Jun 09


Prolonged PGE2 treatment increased TTX-sensitive but not TTX-resistant sodium current in trigeminal ganglionic neurons.



Prostaglandin E (PGE) is an important inflammatory mediator for the initiation and maintenance of inflammatory and neuropathic pain. The acute effect of PGE on sodium currents has been widely characterized in sensory neurons; however, the prolonged effect of PGE remains to be determined. Here, we performed patch clamp recordings to evaluate the acute and prolonged effects of PGE on sodium currents in trigeminal ganglionic (TG) neurons from male Sprague-Dawley rats. We found that 24-h treatment with PGE (10 μM) increased the peak sodium current density by approximately 31% in a voltage-dependent manner and shifted the activation curve in a hyperpolarized direction but did not affect steady-state inactivation. Furthermore, treatment with PGE for 24 h increased the current density of tetrodotoxin-sensitive (TTX-S) but not TTX-resistant (TTX-R) channels significantly. Interestingly, TTX-S current was increased mostly in medium-sized, but not in small-sized, neurons after 24 h of treatment with PGE. Moreover, the mRNA level of TTX-S Nav1.1 but not TTX-R Nav1.8 or Nav1.9 was significantly increased after 24 h of treatment with PGE In contrast, 5-min treatment with PGE (10 μM) increased the peak sodium current density by approximately 29% and increased TTX-R sodium currents, but not TTX-S currents, in both small- and medium-sized TG neurons. Our results presented a differential regulation of subtypes of sodium channels by acute and prolonged treatments of PGE, which may help to better understand the mechanism of PGE-mediated orofacial pain development.