Wang Y T, Neuman R S, Bieger D
Faculty of Medicine, Memorial University of Newfoundland, St. John's, Canada.
Neuroscience. 1991;40(3):759-67. doi: 10.1016/0306-4522(91)90010-l.
The purpose of this study was to determine if ambigual oesophageal motoneurons of the rat possess functional nicotinic cholinoceptors. In urethane anaesthetized rats, acetylcholine (20-50 pmol) delivered micropneumophoretically from multibarrelled pipettes to the compact formation of the nucleus ambiguus produced either synchronous or propulsive oesophageal contractions which were fully and reversibly blocked by dihydro-beta-erythroidine (8-10 pmol) but were resistant to D-tubocurarine and hexamethonium (10-20 pmol). 1,1-Dimethyl-4-phenyl-piperazinium but not muscarine (8 pmol) exerted an analogous agonist action. Ejection of glutamate at the same sites produced similar oesophageal responses which were, however, resistant to dihydro-beta-erythroidine. Acetylcholine applied 5-15 s prior to glutamate transiently facilitated the glutamate-evoked response. The facilitatory effect of acetylcholine was replicated by 1,1-dimethyl-4-phenyl-piperazinium but not muscarine and inhibited by dihydro-beta-erythroidine. Physostigmine, applied either intra-ambigually (10-20 pmol) or by intravenous injection (0.15-0.3 mumol/kg), enhanced both acetylcholine and glutamate-evoked responses. In brainstem transverse slices, application of acetylcholine and glutamate to quiescent ambigual neurons of the compact formation resulted in a rapid membrane depolarization associated with an increased membrane conductance and spiking. Under voltage clamp, both acetylcholine and glutamate elicited a net inward current. The depolarizing response of these neurons to acetylcholine was blocked by dihydro-beta-erythroidine (0.5-2 pmol), hexamethonium (0.2 mM) and D-tubocurarine (10 microM) and persisted in the presence of tetrodotoxin (10(-6) M) or Mn2+ (5 mM) in the bathing medium.(ABSTRACT TRUNCATED AT 250 WORDS)
本研究的目的是确定大鼠的疑核食管运动神经元是否具有功能性烟碱胆碱能受体。在乌拉坦麻醉的大鼠中,用多管移液器微量气动给药乙酰胆碱(20 - 50皮摩尔)至疑核的致密部,可产生同步或推进性食管收缩,这些收缩可被二氢-β-刺桐定(8 - 10皮摩尔)完全且可逆地阻断,但对筒箭毒碱和六甲铵(10 - 20皮摩尔)有抗性。1,1 - 二甲基 - 4 - 苯基哌嗪鎓而非毒蕈碱(8皮摩尔)发挥类似的激动剂作用。在相同部位注射谷氨酸可产生类似的食管反应,然而,该反应对二氢-β-刺桐定有抗性。在谷氨酸注射前5 - 15秒应用乙酰胆碱可短暂促进谷氨酸诱发的反应。乙酰胆碱的促进作用可被1,1 - 二甲基 - 4 - 苯基哌嗪鎓复制,但不能被毒蕈碱复制,且被二氢-β-刺桐定抑制。毒扁豆碱,无论是在疑核内给药(10 - 20皮摩尔)还是静脉注射(0.15 - 0.3微摩尔/千克),均可增强乙酰胆碱和谷氨酸诱发的反应。在脑干横切片中,对致密部静止的疑核神经元应用乙酰胆碱和谷氨酸会导致快速的膜去极化,伴有膜电导增加和放电。在电压钳制下,乙酰胆碱和谷氨酸均引发净内向电流。这些神经元对乙酰胆碱的去极化反应被二氢-β-刺桐定(0.5 - 2皮摩尔)、六甲铵(0.2毫摩尔)和筒箭毒碱(10微摩尔)阻断,且在浴液中存在河豚毒素(10⁻⁶摩尔)或锰离子(5毫摩尔)时持续存在。(摘要截断于250字)