5-HT1A AND 5-HT4 RECEPTORS MEDIATE INHIBITION AND FACILITATION OF FAST SYNAPTIC TRANSMISSION IN ENTERIC NEURONS
5-HT1A AND 5-HT4 RECEPTORS MEDIATE INHIBITION AND FACILITATION OF FAST SYNAPTIC TRANSMISSION IN ENTERIC NEURONS
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DOI：
10.1152/ajpgi.1994.266.2.g230
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发表时间：
1994-02-01
影响因子：
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通讯作者：
GALLIGAN, JJ
中科院分区：
文献类型：
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作者：
PAN, H;GALLIGAN, JJ
本文研究了5-羟色胺(5-HT)(1A)和5-HT4受体激动剂对豚鼠回肠肌间神经元快速兴奋性突触后电位(EPSPS)的作用。采用细胞内电生理方法记录EPSPS。5-羟色胺(0.1mU)、5-氨基色胺(0.001-0.1mU)、8-羟基二丙氨基四氢呋喃(0.003-0.3mU)和5-甲氧基色胺(5-甲氧基色胺；0.3mU)对EPSPS有抑制作用。5-HT1a受体拮抗剂螺环酮和NaN-190可阻断EPSPS的激动剂抑制作用。在NaN-190(0.3mM)存在下，5-羟色胺(0.001-0.1mM)可增加EPSP的幅度。5-MeOT(0.001-0.1mU M)、瑞氮比利(0.01-0.3mU M)、西沙必利(0.01-1mU M)和BIMU-8(0.003-0.1mU M)可增加EPSP幅度，但不改变任何神经元的膜电位。5-HT3/5-HT4受体拮抗剂托烷司琼(1mU M)可阻断5-HT3/5-HT4受体拮抗剂托烷司琼(1mU M)对EPSP的增强作用，但5-HT3受体拮抗剂恩丹西酮(1mU M)不能阻断这一作用。5-羟色胺(0.1mM)对快速EPSP的增强作用不敏感，而瑞氮比利(0.1mU/M)不敏感。BIMU-8诱导的脱敏作用是不同的。这些数据表明，肠道5-HT1a和5-HT4受体分别起抑制和促进递质释放的作用。5-HT4介导的神经节神经传递易化可能参与了西沙必利和雷氮比利的促动力作用。
The actions of 5-hydroxytryptamine (5-HT)(1A) and 5-HT4 receptor agonists on fast excitatory postsynaptic potentials (EPSPs) in myenteric neurons of guinea pig ileum were studied in vitro. Intracellular electrophysiological methods were used to record EPSPs. 5-HT (0.1 mu M), 5-carboxamidotryptamine (0.001-0.1 mu M), 8-hydroxydipropylaminotetralin (0.003-0.3 mu M), and 5-methoxytryptamine (5-MeOT; 0.3 mu M) inhibited EPSPs. Agonist inhibition of EPSPs was blocked by the 5-HT1A receptor antagonists, spiperone and NAN-190. Ln the presence of NAN-190 (0.3 mu M), 5-HT (0.001-0.1 mu M) increased EPSP amplitude. 5-MeOT (0.001-0.1 mu M), renzapride (0.01-0.3 mu M), cisapride (0.01-1 mu M), and BIMU 8 (0.003-0.1 mu M) increased EPSP amplitude but did not change the membrane potential of any neuron. EPSP potentiation induced by each agonist was blocked by the 5-HT3/5-HT4 receptor antagonist, tropisetron (1 mu M), but not by the 5-HT3 receptor antagonist, ondansetron (1 mu M). Potentiation of fast EPSPs by 5-HT (0.1 mu M) desensitized, whereas renzapride (0.1 mu M) responses did not. Desensitization induced by BIMU 8 was variable. These data indicate that enteric 5-HT1A and 5-HT4 receptors function to inhibit and facilitate transmitter release, respectively. 5-HT4-mediated facilitation of ganglionic neurotransmission could contribute to the prokinetic effects of cisapride and renzapride.