Human recombinant interleukin-1 beta inhibits nicotinic transmission in neurons of guinea pig pelvic plexus ganglia.
Human recombinant interleukin-1 beta inhibits nicotinic transmission in neurons of guinea pig pelvic plexus ganglia.
复制标题
人重组白细胞介素 1 β 抑制豚鼠盆腔丛神经节神经元中的烟碱传递。
DOI：
10.1152/ajpgi.1995.269.6.g981
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发表时间：
1995
期刊：
影响因子：
--
通讯作者：
Krier,J
中科院分区：
文献类型：
--
作者：
Lin,J;Krier,J
采用细胞内电生理方法，观察重组人白细胞介素1β(hrIL-1β)对体外培养的豚鼠盆丛神经节神经元的作用。HrIL-1β在54%的受试神经元中引起膜去极化，并伴随着输入电阻或内向电流的减少。HrIL-1β在30%的受试神经元中引起与输入电阻或外向电流增加相关的超极化。六甲铵(100微米)、阿托品(0.5微米)、育亨宾(0.3微米)或纳洛酮(1微米)不改变hrIL-1β诱发的反应，表明胆碱能、α2-肾上腺素能或阿片受体不参与。抑制Na+、Ca2+或K+通道的药物不会改变hrIL-1β诱发的反应。刺激突触传入盆神经节神经元可诱发烟碱胆碱能快速兴奋性突触后电位(FEPSP)。HrIL-1β抑制44%受试神经元的fEPSP，但对乙酰胆碱引起的去极化无影响。IL-1β受体拮抗剂可阻断hrIL-1β的所有作用。综上所述，hrIL-1β对盆神经节神经元具有兴奋和抑制作用。HrIL-1β对fEPSP的抑制可能是由于突触前抑制了乙酰胆碱的释放。
The actions of human recombinant interleukin-1 beta (hrIL-1 beta) were tested on guinea pig pelvic plexus ganglion neurons using intracellular electrophysiological methods in vitro. hrIL-1 beta caused membrane depolarization associated with a decreased input resistance or inward currents in 54% of neurons tested. hrIL-1 beta caused a hyperpolarization associated with an increase in input resistance or outward currents in 30% of neurons tested. hrIL-1 beta-evoked responses were not altered by hexamethonium (100 microM), atropine (0.5 microM), yohimbine (0.3 microM), or naloxone (1 microM), indicating that cholinergic, alpha 2-adrenergic, or opioid receptors were not involved. Drugs that inhibit Na+, Ca2+, or K+ channels did not change hrIL-1 beta-evoked responses. Stimulation of synaptic inputs to pelvic ganglion neurons evoked nicotinic cholinergic fast excitatory postsynaptic potentials (fEPSPs). hrIL-1 beta inhibited fEPSPs in 44% of neurons tested but had no effect on acetylcholine-induced depolarizations. An IL-1 beta receptor antagonist blocked all actions of hrIL-1 beta. In summary, hrIL-1 beta has excitatory and inhibitory actions on pelvic ganglion neurons. Inhibition of fEPSPs by hrIL-1 beta may be due to presynaptic inhibition of acetylcholine release.