Nociceptive receptors are expressed differently in trigeminal nociception after lingual nerve injury and unilateral external carotid artery occlusion in rats

Objectives: To investigate the different changes in nociceptive activity between two animal models of trigeminal neuropathic pain: unilateral external carotid artery ischemic reperfusion and lingual nerve crush in rats. Design: In this study, changes in nociceptive activity were investigated in unilateral external carotid artery ischemic reperfusion and lingual nerve crush models of trigeminal neuropathic pain in rats. Field excitatory postsynaptic potentials (fEPSPs) evoked by capsaicin application on the tongue of rats were recorded in the trigeminal nucleus caudalis. In addition, immunohistochemistry was performed in the trigeminal ganglia and trigeminal nucleus caudalis. Results: The fEPSP in unilateral external carotid artery ischemic reperfusion and lingual nerve crush rats was irregular relative to that in sham rats. In particular, the fEPSP spike in lingual nerve crush rats had a higher amplitude and shorter duration than that in sham rats. Unilateral external carotid artery ischemic reperfusion and lingual nerve crush also increased c-fos expression in the trigeminal nucleus caudalis. Upregulation of transient receptor potential vanilloid 1 in trigeminal ganglion was observed in unilateral external carotid artery ischemic reperfusion and lingual nerve crush rats, whereas upregulation of purinergic receptor subtype 3 in trigeminal ganglion was observed only in lingual nerve crush rats. Conclusions: Although unilateral external carotid artery ischemic reperfusion and lingual nerve crush similarly increased nociceptive activity at the trigeminal nucleus caudalis, the fEPSPs and expression of nociceptive peripheral afferent neurons were different. Therefore, direct and indirect nerve injuries apparently induced the same nociceptive activity by different signaling responses dependent on nociceptive receptors.

Automated summary

The study investigated the changes in nociceptive activity in two animal models of trigeminal neuropathic pain in rats, finding that both unilateral external carotid artery ischemic reperfusion and lingual nerve crush increased nociceptive activity at the trigeminal nucleus caudalis. However, the fEPSPs and expression of nociceptive peripheral afferent neurons differed between the two models.