SELECTIVE DEPRESSION OF EXCITATORY AMINO-ACID INDUCED DEPOLARIZATIONS BY MAGNESIUM-IONS IN ISOLATED SPINAL-CORD PREPARATIONS
SELECTIVE DEPRESSION OF EXCITATORY AMINO-ACID INDUCED DEPOLARIZATIONS BY MAGNESIUM-IONS IN ISOLATED SPINAL-CORD PREPARATIONS
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DOI：
10.1113/jphysiol.1980.sp013443
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发表时间：
1980-01-01
影响因子：
5.5
通讯作者：
WATKINS, JC
中科院分区：
文献类型：
--
作者：
AULT, B;EVANS, RH;WATKINS, JC
在青蛙和新生大鼠脊髓半切离体模型上研究了Mg ~（2+）和一系列其它二价离子对突触兴奋和兴奋性氨基酸及其它假定递质产生的反应的抑制作用。并与大鼠离体上级颈神经节进行了比较研究。在高于10 μ M的浓度下，Mg 2+选择性地拮抗N-甲基-D-天冬氨酸（NMDA）诱导的运动神经元去极化，如从河豚毒素阻断的脊髓的前根记录的。去极化引起的使君子酸（不受20 mM Mg 2+）是耐这些离子的抑制作用，而其他兴奋性氨基酸引起的去极化被压抑到中间程度。Mn 2+、Co 2+和Ni 2+与Mg 2+具有定性相似的作用; Mn 2+的作用略弱，Co 2+和Ni 2+的作用强于Mg 2+。碱土金属离子Ca ~（2+）、Sr ~（2+）和Ba ~（2+）具有很弱的类Mg ~（2+）作用。Ca ~（2+）和Mg ~（2+）对氨基酸诱导的反应有相加抑制作用。Mg ~（2+）还可抑制去甲肾上腺素（norepinephrine）、P物质和卡巴胆碱诱发的新生大鼠离体脊髓运动神经元反应。这些影响都没有明显的抑制NMDA诱导的反应，镁在此制剂。Mg ~（2+）不抑制大鼠脊髓5-HT引起的运动神经元去极化或GABA对离体蛙脊髓初级传入终末的去极化作用。在浓度产生显着的抑郁症的NMDA诱导的反应，Mg 2+也抑制突触传递在脊髓神经节传递的影响的情况下。在相同的浓度下，Mn ~（2+）、Co ~（2+）和Ni ~（2+）在两种制剂中都抑制了突触传递。从Mg 2+和D-α-之间作用的相似性来看，氨基己二酸组的NMDA拮抗剂，这表明，低浓度的Mg ~（2+）的中枢兴奋作用主要涉及突触后介导的干扰兴奋性氨基酸递质的作用。
The depressant actions of Mg2+ and a range of other divalent ions on synaptic excitation and on responses produced by excitatory amino acids and other putative transmitters were investigated in hemisected isolated spinal cords of frogs and neonatal rats. Some comparative studies were also made using the rat isolated superior cervical ganglion. At concentrations above 10 .mu.M, Mg2+ selectively antagonized N-methyl-D-aspartate (NMDA)-induced motoneuron depolarization as recorded from ventral roots of tetrodotoxin-blocked spinal cords. Depolarization evoked by quisqualate (unaffected by 20 mM Mg2+) was resistant to the depressant action of these ions, while depolarizations evoked by other excitant amino acids were depressed to intermediate degrees. Mn2+, Co2+ and Ni2+ had qualitatively similar actions to Mg2+; Mn2+ was somewhat less potent and Co2+ and Ni2+ more potent than Mg2+. The alkaline earth metal ions, Ca2+, Sr2+ and Ba2+, had very weak Mg2+-like actions. Ca2+ and Mg2+ acted additively in depressing amino acid-induced responses. Mg2+ also depressed motoneuron responses evoked by noradrenaline [norepinephrine], substance P and carbachol in the neonatal rat isolated spinal cord. None of these effects were as marked as the depression of NMDA-induced responses by Mg2+ in this preparation. Mg2+ did not depress motoneuron depolarization produced by 5-HT [serotonin] in the rat spinal cord or the depolarizing action of GABA on primary afferent terminals of the isolated frog spinal cord. At concentrations producing marked depression of NMDA-induced responses, Mg2+ also depressed synaptic transmission in spinal cords in the absence of an effect on ganglionic transmission. At the same concentrations, Mn2+, Co2+ and Ni2+ depressed synaptic transmission in both preparations. From the similarity in action between Mg2+ and the D-.alpha.-aminoadipate group of NMDA antagonists, it is suggested that the central depressant action of low concentrations of Mg2+ involves predominantly a postsynaptically mediated interference with the action of an excitatory amino acid transmitter.