Constriction of the buccal branch of the facial nerve produces unilateral craniofacial allodynia

Abstract

Despite pain being a sensory experience, studies of spinal cord ventral root damage have demonstrated that motor neuron injury can induce neuropathic pain. Whether injury of cranial motor nerves can also produce nociceptive hypersensitivity has not been addressed. Herein, we demonstrate that chronic constriction injury (CCI) of the buccal branch of the facial nerve results in long-lasting, unilateral allodynia in the rat. An anterograde and retrograde tracer (3000MW tetramethylrhodamine-conjugated dextran) was not transported to the trigeminal ganglion when applied to the injury site, but was transported to the facial nucleus, indicating that this nerve branch is not composed of trigeminal sensory neurons. Finally, intracisterna magna injection of interleukin-1 (IL-1) receptor antagonist reversed allodynia, implicating the pro-inflammatory cytokine IL-1 in the maintenance of neuropathic pain induced by facial nerve CCI. These data extend the prior evidence that selective injury to motor axons can enhance pain to supraspinal circuits by demonstrating that injury of a facial nerve with predominantly motor axons is sufficient for neuropathic pain, and that the resultant pain has a neuroimmune component.

An Improved Rodent Model of Trigeminal Neuropathic Pain by Unilateral Chronic Constriction Injury of Distal Infraorbital Nerve

“…We noticed that the fluorescence signal from neuronal tracer dextran was detected in the neuron cell bodies in the trigeminal ganglion as early as two days after dextran was applied to the constriction site. It has been reported that when dextran was applied to the buccal nerve branch 15 , the fluorescence signal from dextran tracer was observed in the facial nucleus at 5 days after tracer application. Because the trigeminal nerve is much larger in size compared to the buccal nerve branch, it may take less time for the tracer to reach the neuron cell bodies in the trigeminal ganglion.…”

“…Further studies are needed to evaluate the CVF and SNI-TN models and their role in the study of trigeminal neuropathic pain 20, 30 . Recently, a new animal model was developed to induce facial pain in rats by chronic constriction of the buccal branch of the facial nerve 15 . The rats exhibited both acute and chronic mechanical allodynia after CCI injury 15 .…”

“…Recently, a new animal model was developed to induce facial pain in rats by chronic constriction of the buccal branch of the facial nerve 15 . The rats exhibited both acute and chronic mechanical allodynia after CCI injury 15 .…”

“…Anterograde and retrograde labeling tracer 3000 Da tetramethylrhodamine-conjugated dextran (Invitrogen, Carlsbad, CA, USA) was used to label the neurons in the trigeminal ganglion 15 . The IoN trunk at its distal segment outside the orbital cavity was exposed (Fig 1B).…”

Plasma IL‐8 signature correlates with pain and depressive symptomatology in patients with burning mouth syndrome: Results from a pilot study

“…Pro‐inflammatory cytokines/chemokines are commonly linked with nociceptive signalling and are elevated in neuropathic pain disorders. In terms of orofacial pain, animal studies indicate that IL‐1 signalling mediates allodynia associated with constriction of the buccal branch of the facial nerve, and trigeminal nerve injury has been shown to increase IL‐18 expression (an IL‐1 family member) on microglial cells in the trigeminal spinal nucleus caudalis . Furthermore, inhibition of the TNF‐receptor prevents orofacial thermal and mechanical neuropathic pain in the orofacial region following carrageenan‐induced inflammation and constriction of the infraorbital nerve .…”