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大鼠迷走神经背侧运动神经元缺氧诱导的膜电位变化的离子基础

Ionic basis of membrane potential changes induced by anoxia in rat dorsal vagal motoneurones.

作者信息

Cowan A I, Martin R L

机构信息

Division of Neuroscience, John Curtin School of Medical Research, Australian National University, Canberra, ACT.

出版信息

J Physiol. 1992 Sep;455:89-109. doi: 10.1113/jphysiol.1992.sp019292.

Abstract
  1. The effects of anoxia on membrane properties of 119 dorsal vagal motoneurones (DVMs) were investigated in an in vitro slice preparation of the rat medulla. 2. Membrane potential was unaffected by anoxia in 11% of DVMs. An hyperpolarization accompanied by a decrease in input resistance occurred in 44% of DVMs; the remaining 45% depolarized with either an increase (60%) or decrease in input resistance (40%). TTX at a concentration of 0.3-1 microM did not significantly affect these responses. 3. Anoxic artificial cerebrospinal fluid (ACSF) containing 20 mM-TEA reversed the response of DVMs that hyperpolarized in standard ACSF to reveal a depolarization of 7.4 +/- 2.1 mV, and increased the anoxic depolarization from 5.0 +/- 0.7 to 8.7 +/- 1.4 mV. 4. Anoxic depolarization was converted to an hyperpolarization of 7.3 +/- 2.1 mV in ACSF containing 5 mM-4-aminopyridine (4-AP) and 1 microM-TTX. A residual depolarization of 4.5 +/- 3.5 mV was then observed in ACSF containing 5 mM-4-AP, 1 microM-TTX and 20 mM-TEA. Anoxic hyperpolarization was increased from 7.8 +/- 1.8 to 10.0 +/- 3.9 mV in 5 mM-4-AP and 1 microM-TTX and converted to a depolarization of 5.3 +/- 4.5 mV in 5 mM-4-AP, 1 microM-TTX and 20 mM-TEA. 5. In anoxic ACSF containing TEA, the action potential width was increased from 0.92 +/- 0.04 to 8.1 +/- 1.1 ms in hyperpolarizing DVMs, and from 0.85 +/- 0.01 to 2.4 +/- 1.0 ms in depolarizing DVMs. The increase in width was prevented by 2-3 mM-Mn2+. 6. The long after-hyperpolarization (AHP) of DVMs, which is contributed to by both an apamin-sensitive IK(Ca) and an apamin, charybdotoxin and TEA insensitive IK(Ca) was decreased in duration from 2.59 +/- 0.14 to 1.94 +/- 0.12 s during anoxia. 7. It is concluded that anoxia enhances the delayed rectifier current (IK(DR)) and an inward current, probably ICa, but suppresses the A currents (IA). In DVMs that hyperpolarize during anoxia, the increase in IK(DR) outweighs the increase in ICa and the decrease in IA. In depolarizing DVMs the decrease in IA and increase in ICa outweight the increase in IK(DR). The change in input resistance is determined by the relative sizes of current enhancement or suppression.
摘要
  1. 在大鼠延髓的体外脑片标本中,研究了缺氧对119个迷走神经背运动神经元(DVMs)膜特性的影响。2. 11%的DVMs的膜电位不受缺氧影响。44%的DVMs出现超极化并伴有输入电阻降低;其余45%则去极化,其中输入电阻增加的占60%,降低的占40%。浓度为0.3 - 1微摩尔的河豚毒素(TTX)对这些反应无显著影响。3. 含有20毫摩尔四乙铵(TEA)的缺氧人工脑脊液(ACSF)使在标准ACSF中发生超极化的DVMs的反应逆转,出现7.4±2.1毫伏的去极化,并使缺氧去极化从5.0±0.7毫伏增加到8.7±1.4毫伏。4. 在含有5毫摩尔4 - 氨基吡啶(4 - AP)和1微摩尔TTX的ACSF中,缺氧去极化转变为7.3±2.1毫伏的超极化。然后在含有5毫摩尔4 - AP、1微摩尔TTX和20毫摩尔TEA的ACSF中观察到4.5±3.5毫伏的残余去极化。在5毫摩尔4 - AP和1微摩尔TTX中,缺氧超极化从7.8±1.8毫伏增加到10.0±3.9毫伏,并在5毫摩尔4 - AP、1微摩尔TTX和20毫摩尔TEA中转变为5.3±4.5毫伏的去极化。5. 在含有TEA的缺氧ACSF中,超极化的DVMs的动作电位宽度从0.92±0.04毫秒增加到8.1±1.1毫秒,去极化的DVMs的动作电位宽度从0.85±0.01毫秒增加到2.4±1.0毫秒。动作电位宽度的增加被2 - 3毫摩尔的锰离子(Mn2 +)阻止。6. DVMs的长时超极化后电位(AHP),由一种对蜂毒明肽敏感的IK(Ca)和一种对蜂毒明肽、蝎毒素和TEA不敏感的IK(Ca)共同产生,在缺氧期间持续时间从2.59±0.14秒减少到1.94±0.12秒。7. 得出的结论是,缺氧增强延迟整流电流(IK(DR))和一种内向电流,可能是ICa,但抑制A电流(IA)。在缺氧期间超极化的DVMs中,IK(DR)的增加超过ICa的增加和IA的减少。在去极化的DVMs中,IA的减少和ICa的增加超过IK(DR)的增加。输入电阻的变化由电流增强或抑制的相对大小决定。

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