Establishment An Animal Model In Trigeminal Neuralgia And Study The Electrophysiological Properties Of Neurons In The Caudal Subnucleus Of The Spinal Trigeminal Nucleus

Trigeminal neuralgia (TN) is a recurrent paroxysmal, severe facial pain in thedistribution of one or more branches of the trigeminal nerve. The etiology andpathogenesis of TN is still unclear. In this research, we established an anminal model ofTN induced by chronic compression injury of trigeminal nerve root, which was based onthe clinical common cause of TN by vascular compression. The main results of our studyare as follows:1. Establishment of the rat model of TN16adult male Sprague-Dawley rats (200-220g) were randomly divided into2groups: TN group that received chronic compression of the trigeminal nerve root (n=8),and sham operation group that received sham operation without compression (n=8). Asmall plastic filament was retrogressively inserted into the intracalvarium from theinferior orbital fissure until it reached the trigeminal nerve root for compression in TNgroup. The orofacial mechanical allodynia, heat hyperalgesia and facegrooming behaviorof rats in the TN group were obviously increased after the trigeminal root injury. Inimmunohistochemical staining, glial fibrillary acidic protein (GFAP) positive astrocyticprocesses were progressively proliferated in the ipsilateral trigeminal root entry zone(TREZ) of the TN group, and the positive immunoreactive primary afferent terminals ofisolectin B4(IB4), substance P (SP) and calcitonin gene-related peptide (CGRP) in thecaudal subnucleus of the spinal trigeminal nucleus (Vc) were significantly reduced after the trigeminal nerve root compression injury. These results indicated that chroniccompression of the trigeminal nerve root in rats could effectively induce persistentorofacial neuropathic pain behaviors.2. Whole-cell patch clamp technique for detecting Vc neuronal excitabilityUsing whole-cell patch clamp voltage clamp technique to record the spontaneousexcitatory postsynaptic currents (sEPSCs) of Vc neurons in the rats (TN group, n=6;control group, n=6). The results showed that the frequency and amplitude of sEPSCs ofVc neurons in TN model rats were significantly higher than control group, which impliedthe Vc neuronal excitability was increased in the TN model animal. The enhancedsynaptic transmission mechanism may include both the increase of the presynapticrelease rate and postsynaptic receptor response enhancement.3. The extracellular single-unit recording of Vc neuronal electrophysiologicalproperties in the control group and TN group ratsThe neurons spontaneous discharges and evoked discharges induced by mechanicalstimulation (brush, press, and pinch) in the orofacial receptive field were recorded byextracellular single-unit recording technique in the TN group and control group. Theresults showed that the frequencies of spontaneous discharges and evoked dischargesinduced by mechanical stimulation in TN group were significantly increased.The results in our study showed that, chronic compression injury of the trigeminalnerve root in rats could induce significant mechanical hyperalgesia, thermal hyperalgesiaand spontaneous pain behavior, GFAP positive astrocytic processes were largelyproliferated in the TREZ, both neurotransmitters (SP/CGRP) and IB4expression in Vcneurons were decreased, and Vc neuronal excitability was significantly increased. Ourresults suggested that chronic compression injury of the trigeminal nerve root couldinduce a new reliable animal model of TN in rats.