Abstract
The mechanical head-withdrawal threshold (MHWT) was significantly reduced following inferior alveolar nerve transection (IANX) in rats. Nitrate and nitrite synthesis was dramatically increased in the trigeminal ganglion (TG) at 6 h after the IANX. The relative number of neuronal nitric oxide synthase (nNOS)-immunoreactive (IR) cells was significantly higher in IANX rats compared to sham-operated and N-propyl-L-arginine (NPLA)-treated IANX rats. On day 3 after NPLA administration, the MHWT recovered considerably in IANX rats. Following L-arginine injection into the TG, the MHWT was significantly reduced within 15 min, and the mean number of TG cells encircled by glial fibrillary acidic protein (GFAP)-IR cells was substantially higher. The relative number of nNOS-IR cells encircled by GFAP-IR cells was significantly increased in IANX rats. In contrast, after NPLA injection into the TG, the relative number of GFAP-IR cells was considerably reduced in IANX rats. Fluorocitrate administration into the TG significantly reduced the number of GFAP-IR cells and prevented the MHWT reduction in IANX rats. The present findings suggest that following IANX, satellite glial cells are activated via nitric oxide (NO) signaling from TG neurons. The spreading satellite glial cell activation within the TG results in mechanical hypersensitivity of face regions not directly associated with the trigeminal nerve injury.
Highlights
It is well known that ectopic orofacial pain occurs after trigeminal nerve injuries such as tooth extraction, tooth pulpectomy, maxillofacial bone fractures, or orofacial cancers [1]
Mechanical stimulation was applied to the whisker pad skin, ipsi- or contralateral to the site of thMe eIcAhNanXicoarl ssthimamulasutirognerwya(sFaigpuprleie1d).toThtheemwehcihsakneircapladhesakdi-nw, iitphsdi-raowr acol nthtrraelsahtoerldaltewas of thsiegInAifNicXanotlryslhoawmersuinrgIAerNyX(Friagtusrfeor1)1.–T5hdeamfteecrhIAanNicXalchomeapda-rweidthtodrtahwe palreth-orpesehraotlidon(MvaHluWeTip) swilaasteral signtiofitchaentIlAyNloXw(eFriginurIAe 1NaX) arnadts ifposril1a–t5erdalatfotetrhIeAsNhaXmcoompepraarteiodntowtahsespurbes-toapnetriaaltliyonlovwaelureinipsshilaamterraalts at to th1edIAafNteXr s(uFrigguerrye.1Wa)eadniddinpositloatbesrearlvteoatnhye schhaamngoeps einraMtioHnWwTasonsutbhsetasindteiaclloynltorawlaetreirnalshtoamtheraIAtsNatX or 1 d ashftaemr ssuurgrgeeryry. .We did not observe any changes in mechanical head-withdrawal threshold (MHWT) on the side contralateral to the IANX or sham surgery
We studied double immunohistochemistry with neuronal nitric oxide synthase (nNOS)-IR and glial fibrillary acidic protein (GFAP)-IR cells in the trigeminal ganglion (TG). nNOS-IR cells encircled by GFAP-IR cells were counted in the TG of sham-operated and IANX rats, and the relative number of nNOS-IR cells encircled by GFAP-IR cells was calculated
Summary
It is well known that ectopic orofacial pain occurs after trigeminal nerve injuries such as tooth extraction, tooth pulpectomy, maxillofacial bone fractures, or orofacial cancers [1]. Injury-induced neuronal discharges occur after nerve damage [2], and high-frequency spikes are generated in both uninjured and injured nerve fibers [3]. Spontaneous spike discharges in uninjured nerve fibers last more than 1 week after nerve injury [3]. Takeda et al reported that after temporomandibular joint inflammation, substance P (SP) production is enhanced in small-diameter TG neurons, which release SP via a paracrine mechanism [7]. This SP binds to neurokinin-1 (NK1) receptors expressed by uninjured TG neurons, resulting in their enhanced excitability [7]. Various chemokines are known to be released from injured TG neurons and are involved in the modulation of the excitability of uninjured TG neurons [8]
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