论文部分内容阅读
应用细胞外记录单位放电技术,在大鼠下丘脑脑片上观察了尾加压素Ⅱ(urotensinⅡ)对下丘脑室旁核(paraventricular nucleus,PVN)神经元放电的影响。实验结果如下:(1)在39个PVN神经元放电单位给予尾加压素Ⅱ(0.3,3.0,30.0,300.0nmol/L,n=39)2min,有32个放电单位(82.05%)放电频率明显降低,且呈剂量依赖性;(2)预先用100μmol/L的GABAA受体拮抗剂荷包牡丹碱灌流7个下丘脑脑片,5个放电单位放电频率明显增加(71.43%),在此基础上灌流尾加压素Ⅱ(30.0nmol/L)2min,放电频率无明显变化;(3)预先用氯通道阻断剂印防己毒素(picrotoxin)灌流12个下丘脑脑片,12个放电单位的放电频率均明显增加(100%),在此基础上灌流尾加压素Ⅱ(30.0nmol/L)2min,11/12(91.67%)放电频率无变化;(4)12个放电单位灌流一氧化氮合酶抑制剂(NG-nitro-L-arginine methylester,L-NAME)50μmol/L,有11个单位(11/12,91.67%)放电明显增加,在此基础上灌流尾加压素Ⅱ(30.0nmol/L)2min,放电被抑制。以上结果提示:尾加压素Ⅱ能抑制下丘脑室旁核神经元自发放电,可能与其同GABAA受体结合加强氯电流有关。
The effect of urotensin Ⅱ on the discharge of neurons in the paraventricular nucleus (PVN) of the hypothalamus was observed in rat hypothalamic slices using extracellular recording unit discharge technique. The experimental results are as follows: (1) There were 32 discharge units (82.05%) discharge frequency in 39 PVN neuron discharge units (2 × 10,3.0,30.0,300.0nmol / L, n = 39) (2) Seven hypothalamic slices were perfused with 100μmol / L GABAA receptor antagonist bicuculline, and the firing rate of five discharge units increased significantly (71.43%). Based on this, After perfusing urotensin Ⅱ (30.0nmol / L) for 2min, there was no significant change in the discharge frequency. (3) Twelve hypothalamic slices were previously perforated with picrotoxin, a chloride channel blocker, with 12 discharge units (100%). On the basis of this, urinary urotensin Ⅱ (30.0nmol / L) was added for 2min and the discharge frequency of 11/12 (91.67%) did not change. (4) There were 11 units (11 / 12,91.67%) of 50nmol / L N-nitro-L-arginine methylester (L-NAME) discharge significantly increased discharge on the basis of urotensin Ⅱ 30.0nmol / L) for 2min, the discharge was inhibited. These results suggest that: Urotensin II can inhibit spontaneous discharge of hypothalamic paraventricular nucleus neurons, which may be related to the GABAA receptor to strengthen the chloride current.