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机构地区:[1]华中科技大学同济医学院附属协和医院耳鼻咽喉科
出 处:《中华耳鼻咽喉头颈外科杂志》2005年第11期830-834,共5页Chinese Journal of Otorhinolaryngology Head and Neck Surgery
基 金:国家杰出青年基金资助项目(39925035);国家自然科学基金资助项目(30070809);教育部高等学校骨干教师资助计划(200065)
摘 要:目的探讨γ氨基丁酸(γaminobutyricacid,GABA)不同受体在前庭核神经元电活动调控中的作用。方法选用健康雄性Wistar大鼠26只,以在体微电泳方法检测γ氨基丁酸、荷包牡丹碱(bicuculine,BIC,γ氨基丁酸A拮抗剂)和2羟基巴氯芬(2hydroxysaclofen,SAC,γ氨基丁酸B拮抗剂)对大鼠前庭内侧核神经元自发放电的影响。结果记录了42个前庭内侧核神经元对γ氨基丁酸的反应,以10、30、50nA的电流微电泳γ氨基丁酸,放电频率的减少呈明显的量效关系,平均放电频率(x±s)由基础频率的(14.8±5.6)次/s分别减至(8.7±3.4)次/s、(4.1±1.6)次/s和(2.2±1.1)次/s;观察了37个前庭内侧核神经元对BIC的反应,微电泳BIC后,86.5%(32/37)神经元出现兴奋性反应,13.5%(5/37)无反应;以10、30、50nA的电流电泳BIC,放电频率分别由基础状态下的(15.3±6.3)次/s分别增加至(16.8±7.1)次/s、(25.9±10.1)次/s和(32.7±11.3)次/s,呈明显的量效关系,并能完全阻断γ氨基丁酸的抑制性效应;但微电泳SAC对大多数前庭内侧核神经元无明显影响,对γ氨基丁酸的阻断作用也不明显。结论γ氨基丁酸能明显抑制前庭内侧核神经元自发放电,这种作用主要是通过γ氨基丁酸A受体介导的。Objective To investigate modulation of γ-aminobutyric acid (GABA) and its receptors on medial vestibular nucleus neurons in vivo. Methods Twenty-six male Wistar rats were used. γ-aminobutyric acid,bicuculine (BIC, γ-aminobutyric acid A receptor antagonist) and 2-hydroxysaclofen (SAC, γ-aminobutyric acid B receptor antagonist) were microiontophoreted on medial vestibular nucleus (MVN) neurons to determine the effects of γ-aminobutyric acid and its antagonists on the neuronal firing rates of medial vestibular nucleus in rats in vivo. Results Microiontophoretic application of γ-aminobutyric acid at 10, 30, 50 nA electric current produced inhibitory responses on 42 MVN neurons, these responses were dose-dependent decreases, firing rates (x^-± s ) of MVN neurons decreased form ( 14. 8 ± 5.6 ) times/s to (8.7 ±3.4) times/s, (4. 1 ± 1. 6) times/s and (2.2± 1.1 ) times/s respectively; microiontophoretic application of bicuculine in 37 MVN neurons, 86. 5% (32/37) neurons produced excitatory responses, 13.5% (5/37) neurons didn't responsed, firing rates of MVN neurons increased form ( 15.3 ±6. 3) times/s to ( 16. 8 ± 7. 1 ) times/s, (25.9 ± 10. 1 ) times/s and (32. 7 ± 11.3) times/s respectively at 10, 30, 50 nA electric current, which were dose-dependent increases, and the inhibitory responses of γ-aminobutyric acid on MVN neurons were blocked by bicuculine completely; however, microiontophoretic application of 2-hydroxysaclofen didn't produced responses as bicuculine did. Conclusions Modulation of γ-aminobutyric acid on medial vestibular nucleus neurons was mediated by γ-aminobutyric acid A receptor in vivo.
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