精氨酸加压素反转前列腺素E_2引起的大鼠视前区冷敏神经元活性增强

Study on the Reversing Effect of Arginine Vasopressin on the Prostaglandin E_2-induced Enhancement of the Activity of Cold-sensitive Neurons in the Preoptic Area of Rats

目的研究精氨酸加压素(AVP)对前列腺素E2(PGE2)引起大鼠视前区冷敏神经元活性变化的影响。方法在制作了大鼠视前区脑片以后,应用全细胞膜片钳技术记录视前区神经元的放电频率,鉴别它们的温度敏感性,然后分别记录PGE2(1μmol)、AVP(1μmol)+PGE2(1μmol)或AVP(1μmol)+PGE2(1μmol)+AVP V1a受体阻断剂(1μmol)对冷敏神经元放电频率的影响。结果 1)加入PGE2后,有61.5%(8/13)的大鼠视前区冷敏神经元的放电频率明显上升,其平均增幅为(69.6±39.7)%。2)洗脱PGE2的作用后,往PGE2激活的冷敏神经元浴液中加入了PGE2和AVP混合液后,这些神经元的平均放电变化却转为下降(P<0.05),说明AVP反转了PGE2引起的冷敏神经元放电活性增强。3)洗脱PGE2和AVP混合液的作用后,继续加入了PGE2、AVP和AVP V1a受体拮抗剂,神经元的平均放电变化与PGE2和AVP混合液引起的放电变化差异有统计学意义(P<0.05),而且与PGE2引起的放电变化相似(P>0.05),表明AVP V1a受体拮抗剂阻断了AVP对PGE2引起冷敏神经元放电频率变化的影响。结论 PGE2可引起大鼠视前区冷敏神经元活性增强,AVP通过激活V1a受体反转了PGE2引起的冷敏神经元活性增强。

Objective To investigate the reversing effect of Arginine vasopressin （AVP） on the prostaglandin E 2 （PGE 2）-induced change in the activity of cold-sensitive neurons in the preoptic area of rats. Methods The whole-cell patch clamp technique was used to record the discharge frequency of the neurons of the preoptic area and identify their thermosensitivity after the preparation of the brain slices of the rat＇s preoptic area, and then the effect of PGE 2 （1μmol）, AVP （1μmol） ＋ PGE 2 （1μmol）, and AVP （1μmol） ＋ PGE 2 （1μmol） ＋ AVP V 1a receptor antagonist （1μmol） on the discharge frequency of cold-sensitive neurons were recoded respectively. Results Firstly, after the application of PGE 2, the discharge frequency of 61.5% （8/13） of cold-sensitive neurons in the rat＇s preoptic area increased obviously with the average growth of （69.6±39.7）%. Secondly, after the elution of PGE 2 effect and the perfusion of PGE 2 and AVP into the bath preparation of PGE 2-activated cold-sensitive neurons, the discharge frequency of those neurons was decreased significantly （ P 〈0.05）, which indicated that AVP reversed the PGE 2-induced enhancement of the discharge frequency of cold-sensitive neurons. Thirdly, after the elution of the PGE 2 and AVP effect and the perfusion of PGE 2, AVP and AVP V 1a receptor antagonist, the discharge frequency of the neurons was significantly different from that in the mixture of PGE 2 and AVP （ P 〈0.05） and it was similar with that in the mixture of PGE 2 （ P 〉0.05）, which indicated that the AVP V 1a receptor antagonist blocked the effect of AVP on the PGE 2-induced change in the discharge frequency of cold-sensitive neurons. Conclusion PGE 2 could enhance the activity of cold-sensitive neurons in the preoptic area of rats; AVP reversed the PGE 2-induced enhancement of the activity of cold-sensitive neurons by activating the AVP V 1a receptor.