Citicoline Administration Increases the Brain-derived Neurotrophic Factor (Bdnf) Expression in the Trigeminal Ganglion of Rats Post-mental Nerve Injury

The number of neurons in the sensory ganglion decreases after a peripheral nerve injury (PNI) caused by oral trauma or maxillofacial surgery, resulting in an incomplete nerve regeneration process. Thus, there is an urgent need to reduce the risk for potential complications after PNI, including neuropathic/ectopic pain and allodynia. Citicoline administration reportedly can improve motor function and prevent neuropathic pain in a rat model of PNI. Therefore, the present study aimed to assess the effect of citicoline administration on Brain-derived neurotrophic factor (Bdnf) expression, which is an early indicator of an ongoing nerve regeneration process, and the number of trigeminal neurons at the chronic phase after a PNI in a rat model. The PNI model was established by clamping the mental nerve of Wistar rats with a non-serrated clamp for 30 s. The animals were divided into the following three groups: sham-operated; clamp-injured rats receiving saline as the controls; and clamp-injured rats receiving a daily dose citicoline 50 mg/100g body weight intraperitoneally immediately after surgery for 7 days. They were sacrificed on days 1,3, and 7 for the acute phase analysis to examine the changes in Bdnf expression using quantitative reverse transcriptio polymerase chain reaction. Subsequently, the chronic phase analysis was done by counting the neuron number in the trigeminal ganglion on day 28 post-injury using the stereological method. In the acute phase, citicoline administration increased the Bdnf expression by 2.19 times only on the third-day post-injury, indicating the start of an early regenerative process. However, in the chronic phase, the total number of neurons in the trigeminal ganglion remained similar in all groups, suggesting the possibility of inadequate injury level. In conclusion, although there was no neuronal loss after a mental nerve injury, citicoline administration increased the Bdnf expression at the trigeminal ganglion immediately after the nerve injury, and this may accelerate nerve regeneration.