The Role Of BNP/BKCa Pathway In Trigeminal Neurons Of Trigeminal Neuralgia Rats

Objective The trigeminal neuralgia model was established by suborbital nerve compression(ION-CCI)in SD rats.The role of BNP/ BKCa pathway in trigeminal ganglion neurons of rat trigeminal neuralgia model was investigated by behavioral examination and patch clamp technique.Methods Sixty normal SD rats(120-150 g)were randomly divided into two groups:Sham group(n = 5)and ION-CCI group(n = 5).The rats were fed adaptively and stimulated for 5 days.The normal rats with calm and healthy response to a certain amount of stimulation were selected and randomly divided into two groups: ION-CCI group(n = 5)and control group(n = 5).The mechanical pain thresholds of the two groups were measured and compared by von Frey hair at the palpation pad of rats.After the successful establishment of the model,the rats in the corresponding group were decapitated on the 7th day after anesthesia.The neuronss were isolated from the trigeminal ganglion and detected with patch clamp in Sham group,ION-CCI group,Sham group + Paxilline,ION-CCI + BNP group.The current densities of BKca channel were recorded in all groups.The data were analyzed statistically to explore the role of BNP/BKCa pathway in pain model..Results 1.The results showed that the mechanical pain thresholds of ION-CCI group were significantly lower than that of Sham group,and reached the lowest value on the7 th day.(Sham group:(1.64 ± 0.14)g;ION-CCI group:(0.10 ± 0.02)g;n = 5,P <0.0001)2.The current density of BKCa in normal trigeminal neurons was 302.10 ± 30.59pA/pF(n = 5),and after treated with 1 ?mol/L paxilline,the current density of BKCa in trigeminal neurons was 169.70 ± 19.93 pA/pF(n = 5).There was significant difference between the two groups(P < 0.05).3.When the stimulation voltage reached + 40 mV,the current density of BKCa in trigeminal neurons was 463.40 ±19.11 pA/pF in the sham group(n = 5),and was 235.9±12.33 pA/pF in the ION-CCI group(n = 5).There was significant difference between the two groups(P < 0.05).4.When the stimulation voltage reached + 50 mV,the current density of BKCa in trigeminal neurons was 561.30 ±29.14 pA/pF in the sham group(n = 5).After treated with 100 ng/ml BNP,the current density of BKCa in trigeminal neurons was 725.90±59.77 pA/pF in the sham group(n = 5).There was significant difference between the two groups(P < 0.05).5.When the stimulation voltage reached + 40 mV,the current density of BKCa in trigeminal neurons was 209.80 ±23.70 pA/pF in the ION-CCI group(n = 5).After treated with 100 ng/ml BNP,the current density of BKCa in trigeminal neurons was310.70 ±36.64 pA/pF in the ION-CCI group(n = 5).There was significant difference between the two groups(P < 0.05).6.After treated with BNP(100ng/ml,1min),the current density of BKCa was increased about 22.33%(n = 5)in the sham group.After treated with BNP(100ng/ml,1min),the current density of BKCa increased by 31.45% in the ION-CCI group(n ? 5).There was significant difference between the two groups(P < 0.05).Conclusion In the rat model of trigeminal neuralgia established by chronic infraorbital nerve compression,the current density of BKCa is significantly decreased,and BNP can improve the opening rate of BKCa.These results suggest that BNP/BKCa signaling pathway may be involved in the occurrence and development of trigeminal neuralgia inrats and play a role in pain regulation.