水杨酸钴镍作用下海马ca3区总生物电位的频幅特征

D. Khusainov, E. Chuyan, I. I. Korenyuk, V. L. Ablyakimova
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引用次数: 0

摘要

用10-2 M、10-3 M、10-4 M和10-6 M浓度的水杨酸钴和镍溶液灌注大鼠海马断面,研究了水杨酸钴和镍的嗜神经作用。本研究结果令人信服地证明,乙酰水杨酸与二价金属钴和镍的络合盐的形成导致了不同程度的神经作用变化。在水杨酸镍的情况下,与乙酰水杨酸和水杨酸相比,抑制性嗜神经效应的严重程度有所降低[16]。而当水杨酸钴浓度为10-4 M时,则表现出活化效应。我们认为这是由于整个络合物的影响,因为水杨酸钴表现出高度的稳定性,特别是在水溶液中[10]。这种盐应该保持相当稳定。在这方面,很自然地假设与酸相比,水杨酸钴能够触发其他过程,并且可能其作用机制与COX系统的关联不那么强。所观察到的激活效应可能与对神经细胞的直接刺激作用和/或神经网络中同步兴奋的结果有关。值得注意的是,这项研究揭示的水杨酸钴的嗜神经作用与这种盐对葡萄蜗牛咽下神经节复合体神经元功能的影响方向一致[10]。这表明这种盐对无脊椎动物和脊椎动物神经组织的影响机制是一致的。对于水杨酸镍,与前体酸相比,只有抑制作用减弱,可能是该盐的稳定常数不高,发生了明显的解离。因此,乙酰水杨酸释放的残基会阻断COX,从而触发一种类似于盐溶液作用的嗜神经影响机制,其作用已在前面介绍过[16]。镍离子的贡献将是微不足道的,因为它在盐分子中的质量分数很小。从离子机制的角度来看,我们认为所研究的盐对总生物电位产生的抑制很可能与抑制进入的钠电流有关。而水杨酸钴在浓度为10-4 M时的刺激作用则相反,随其刺激(缓解)。此外,所描述的效应可以作为神经网络中突触相互作用调节的结果来实现。阐明这些生物物理机制是我们进一步研究的首要任务。此外,最重要的问题仍然是,这些盐在不同的物质注射到体内时的效果可能发生的变化:口服、肌肉注射、静脉注射等。
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FREQUENCY-AMPLITUDE CHARACTERISTICS OF THE TOTAL BIOPOTENTIALS OF THE CA3 ZONE OF THE HIPPOCAMPUS UNDER THE ACTION OF COBALT AND NICKEL SALICYLATE
The neurotropic effects of cobalt and nickel salicylate were studied during perfusion of rat hippocampal sections with solutions of these salts at concentrations of 10-2 M, 10-3 M, 10-4 M and 10-6 M. The results of this study convincingly demonstrate that the formation of complex salts of acetylsalicylic acid with divalent metals cobalt and nickel leads to changes in neurotropic effects with varying degrees of severity. In the case of nickel salicylate, there is a decrease in the severity of the depressing neurotropic effect compared with acetylsalicylic and salicylic acids [16]. And in the case of cobalt salicylate at a concentration of 10-4 M, an activation effect is manifested. We believe that this is due to the influence of the whole complexon, since a high degree of stability is shown for cobalt salicylate, especially in an aqueous solution [10]. And this salt should remain fairly stable. In this regard, it is natural to assume that cobalt salicylate is capable of triggering other processes compared to acids and, perhaps, the mechanism of its action is less strongly associated with the COX system. The observed activation effect may be associated with a direct stimulating effect on the nerve cell and/or the result of synchronization of excitation in neural networks. It should be noted that the neurotropic effects of cobalt salicylate revealed in this work coincide in their orientation with the effect of this salt on the functioning of neurons of the subcaryngeal ganglia complex of the grape snail [10]. This indicates the uniformity of the mechanisms of influence of this salt on the nervous tissue of invertebrates and vertebrates. For nickel salicylate, only a weakening of the inhibitory effect is shown in comparison with the precursor acids, perhaps the stability constant of this salt is not high and its noticeable dissociation occurs. As a result, the released residues of acetylsalicylic acid will block COX, which will trigger a mechanism of neurotropic influence close to the effects of salt solutions, the effects of which were described earlier [16]. The contribution of nickel ions will be insignificant, because its mass fraction in the salt molecule is small. From the position of ionic mechanisms, we believe that the inhibition of the generation of total biopotentials by the studied salts is most likely associated with the suppression of the incoming sodium current. And the stimulating effect of cobalt salicylate in a concentration of 10-4 M, on the contrary, with its stimulation (relief). Also, the described effects can be realized as a result of modulation of synaptic interaction in neural networks. Elucidation of these biophysical mechanisms is a priority task of our further research. And also, the most important question remains open about the possible change in the effects of these salts with different injections of substances into the body: oral, intramuscular, intravenous, etc.
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