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关于钙和镁影响哺乳动物运动神经末梢递质自发释放的机制

On the mechanism by which calcium and magnesium affect the spontaneous release of transmitter from mammalian motor nerve terminals.

作者信息

Hubbard J I, Jones S F, Landau E M

出版信息

J Physiol. 1968 Feb;194(2):355-80. doi: 10.1113/jphysiol.1968.sp008413.

Abstract
  1. The frequency of miniature end-plate potentials (m.e.p.p.s) was recorded from neuromuscular junctions in rat diaphragm phrenic nerve preparations in vitro after preparations had soaked in solutions containing Ca in concentrations between 10(-10) and 10(-2)M and a similar range of [Mg].2. Ethylenediamine tetra-acetate (EDTA) and ethyleneglycol bis (beta-aminoethyl ether) tetra-acetate (EGTA) buffers were added to prepare solutions with [Ca] and [Mg] below 10(-4)M. A computer program was used to estimate the free [Ca(2+)] in these solutions, and it was shown that the effects of Ca could be attributed to the free [Ca(2+)] in the bathing solution.3. M.e.p.p.s could still be detected without difficulty after soaking preparations for 6-8 hr in solutions containing EDTA or EGTA buffers and no added Ca. The basal frequency was unchanged upon exhibition of Ca in concentrations up to 10(-5)M and/or Mg in concentrations up to 10(-3)M.4. Ca in concentrations of and above 10(-4)M accelerated m.e.p.p. frequency from the basal level. This effect reached a maximum in [Ca] of 10 mM and raising the [Ca] above this level did not further change frequency. These effects were explained by the combination of Ca molecules with a nerve terminal receptor site. It was postulated that this combination allosterically activated the spontaneous release mechanism.5. Mg could accelerate m.e.p.p. frequency in the absence of added Ca. The interactions of Ca and Mg upon m.e.p.p. frequency indicated that Ca and Mg competed for the same sites.6. Raising the [H(+)] of the bathing medium accelerated m.e.p.p. frequency. This effect was thought to be exerted partly by combination with the same receptor sites as Ca and Mg and partly by variation of the ionization of the CaCl(2) of the bathing solution.
摘要
  1. 将大鼠膈神经膈肌标本浸泡于含有浓度在10⁻¹⁰至10⁻²M之间的钙以及类似浓度范围镁的溶液中后,在体外记录大鼠膈神经膈肌标本神经肌肉接头处微小终板电位(m.e.p.p.s)的频率。

  2. 添加乙二胺四乙酸(EDTA)和乙二醇双(β - 氨基乙醚)四乙酸(EGTA)缓冲剂以制备钙和镁浓度低于10⁻⁴M的溶液。使用计算机程序估算这些溶液中的游离[Ca²⁺],结果表明钙的作用可归因于浴液中的游离[Ca²⁺]。

  3. 将标本在含有EDTA或EGTA缓冲剂且未添加钙的溶液中浸泡6 - 8小时后,仍能轻松检测到m.e.p.p.s。在高达10⁻⁵M的钙浓度和/或高达10⁻³M的镁浓度下,基础频率未发生变化。

  4. 浓度为10⁻⁴M及以上的钙可使m.e.p.p.频率从基础水平加速。此效应在[Ca]为10 mM时达到最大值,将[Ca]提高到该水平以上不会进一步改变频率。这些效应可通过钙分子与神经末梢受体位点的结合来解释。据推测,这种结合通过变构激活了自发释放机制。

  5. 在未添加钙的情况下,镁可加速m.e.p.p.频率。钙和镁对m.e.p.p.频率的相互作用表明,钙和镁竞争相同的位点。

  6. 提高浴液介质的[H⁺]可加速m.e.p.p.频率。这种效应被认为部分是通过与钙和镁相同的受体位点结合,部分是通过改变浴液中CaCl₂的电离来实现的。

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