Involvement of the NMDA-Nitric Oxide Pathway in the Development of Hypersensitivity to Tactile Stimulation in Dental Injured Rats.

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Abstract

To investigate mechanisms in pathological pain conditions as the hyperalgesia and allodynia observed after dental surgery, we employed a rat dental-injury model involving the simultaneous pulpectomy to a lower incisor and extraction of an ipsilateral upper incisor. We found that hypersensitivity to tactile stimulation developed on both ipsilateral and contralateral sides in the dental-injured rats 5 days after the surgery and that this lasted for at least 30 days. Recovery from hypersensitivity to tactile stimulation was achieved by the intraperitoneal (i.p.) administration of MK-801 (0.05 mg/kg) or NG-monomethyl-<sc>L</sc>-arginine monoacetate (<sc>L</sc>-NMMA: 10 – 100 mg/kg), but not attained by NG-monomethyl-<sc>D</sc>-arginine monoacetate (<sc>D</sc>-NMMA: 100 mg/kg). This recovery effect of <sc>L</sc>-NMMA (50 mg/kg) was inhibited by pretreatment with <sc>L</sc>-arginine (600 mg/kg). In the trigeminal nucleus caudalis (SpVc), the changes in nitric oxide (NO) levels invoked by the intravenous (i.v.) administration of N-methyl-<sc>D</sc>-aspartate (NMDA; 10 mg/kg) were found to be significantly larger in the dental-injured rats than in sham-operated rats. The number of neuronal NO synthase (nNOS)-positive neurons increased in layers I-II and III-IV in the SpVc on both sides of the dental-injured rats. These results suggest that hypersensitivity to tactile stimulation developed following dental injury, and that NMDA receptor/NOS/NO production pathways in the SpVc may be involved in pathological conditions.<br>

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