Lin J, Krier J
Department of Physiology, Michigan State University, East Lansing 48824, USA.
Am J Physiol. 1995 Dec;269(6 Pt 1):G981-7. doi: 10.1152/ajpgi.1995.269.6.G981.
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.
利用细胞内电生理方法在体外对豚鼠盆腔神经丛神经节神经元检测了人重组白细胞介素 -1β（hrIL -1β）的作用。在54%的被检测神经元中，hrIL -1β引起膜去极化，伴有输入电阻降低或内向电流。在30%的被检测神经元中，hrIL -1β引起超极化，伴有输入电阻增加或外向电流。六甲铵（100微摩尔）、阿托品（0.5微摩尔）、育亨宾（0.3微摩尔）或纳洛酮（1微摩尔）不改变hrIL -1β诱发的反应，表明不涉及胆碱能、α2 -肾上腺素能或阿片样物质受体。抑制钠、钙或钾通道的药物不改变hrIL -1β诱发的反应。刺激盆腔神经节神经元的突触输入诱发烟碱型胆碱能快速兴奋性突触后电位（fEPSPs）。hrIL -1β在44%的被检测神经元中抑制fEPSPs，但对乙酰胆碱诱导的去极化无影响。白细胞介素 -1β受体拮抗剂阻断hrIL -1β的所有作用。总之，hrIL -1β对盆腔神经节神经元有兴奋和抑制作用。hrIL -1β对fEPSPs的抑制可能是由于对乙酰胆碱释放的突触前抑制。
