尾加压素Ⅱ对大鼠下丘脑室旁核神经元放电的影响(英文)

EFFECTS OF UROTENSIN II ON ELECTRICAL ACTIVITY OF PARAVENTRICULAR NEURONS IN RAT HYPOTHALAMIC SLICES

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。

Effects of urotensin Ⅱ （UⅡ） on paraventricular nucleus （PVN） neurons of hypothalamus from brain slices of rats were examined by using extracellular recording technique. The results are as follows： （ 1 ） In response to application of UⅡ （0.3, 3.0, 30.0,300. 0 nmol/L, n = 39） into the perfusate for 2 rain, the spontaneous discharge rates （SDR） of 32/39 （ 82.05 % ） neurons were significantly decreased in a dose-dependent manner; （2） Pretreatment with bicuculline （BIC, 100 μmol/L）, a specific GABAA receptor antagonist, led to a marked increase in SDR of 5/7 （ 71.43% ） neurons in an epileptiform pattern. The increased discharges were not significantly changed after UⅡ （ 30.0 nmol/L ） was applied into the perfusate for ：2 rain; （3） Pretreatment with picrotoxin （ PIC, 50 μmol/L ） , a selective blocker of Cl^- channel, led to an increase in the SDR of all 12/12 （ 100% ） neurons. The increased discharges were not influenced by the applied UⅡ （30.0 nmol/L） for 2 rain in 11/12 （91.67%） neurons; （4） Application of nitric oxide synthase （NOS） inhibitor NC-nitro-L-arginine methyl ester （L-NAME, 50 μmol/L ） into the perfusate could significantly augment the SDR of 11/12 （ 91.67% ） neurons , while UⅡ （ 30.0 nmol/L ） applied into the perfusate for 2 rain led the augmented SDR of all （ 12/12, 100% ） neurons decrease. The results suggest that UⅡ decreases the excitability of PVN neurons of hypothalamus by potentiating GABAA receptor-mediated Cl^- current.