Zinchenko Valery Petrovich, Kosenkov Artem Mikhailovich, Gaidin Sergei Gennadevich, Sergeev Alexander Igorevich, Dolgacheva Ludmila Petrovna, Tuleukhanov Sultan Tuleukhanovich
Federal Research Center "Pushchino Scientific Center for Biological Research of the Russian Academy of Sciences", Institute of Cell Biophysics of the Russian Academy of Sciences, 142290 Pushchino, Russia.
Laboratory of Biophysics, Chronobiology and Biomedicine, Faculty of Biology and Biotechnology, Al-Farabi Kazakh National University, Almaty 050040, Kazakhstan.
Life (Basel). 2021 Nov 27;11(12):1309. doi: 10.3390/life11121309.
Calcium-permeable kainate and AMPA receptors (CP-KARs and CP-AMPARs), as well as NMDARs, play a pivotal role in plasticity and in regulating neurotransmitter release. Here we visualized in the mature hippocampal neuroglial cultures the neurons expressing CP-AMPARs and CP-KARs. These neurons were visualized by a characteristic fast sustained [Ca] increase in response to the agonist of these receptors, domoic acid (DoA), and a selective agonist of GluK1-containing KARs, ATPA. Neurons from both subpopulations are GABAergic. The subpopulation of neurons expressing CP-AMPARs includes a larger percentage of calbindin-positive neurons (39.4 ± 6.0%) than the subpopulation of neurons expressing CP-KARs (14.2 ± 7.5% of CB neurons). In addition, we have shown for the first time that NHCl-induced depolarization faster induces an [Ca] elevation in GABAergic neurons expressing CP-KARs and CP-AMPARs than in most glutamatergic neurons. CP-AMPARs antagonist, NASPM, increased the amplitude of the DoA-induced Ca response in GABAergic neurons expressing CP-KARs, indicating that neurons expressing CP-AMPARs innervate GABAergic neurons expressing CP-KARs. We assume that CP-KARs in inhibitory neurons are involved in the mechanism of outstripping GABA release upon hyperexcitation.
钙通透性海人酸受体和α-氨基-3-羟基-5-甲基-4-异恶唑丙酸受体（CP-KARs和CP-AMPARs）以及N-甲基-D-天冬氨酸受体（NMDARs）在可塑性和调节神经递质释放中起关键作用。在此，我们在成熟的海马神经胶质细胞培养物中观察到了表达CP-AMPARs和CP-KARs的神经元。这些神经元通过对这些受体的激动剂——软骨藻酸（DoA）以及含GluK1的KARs的选择性激动剂——ATPA产生特征性的快速持续性[Ca]升高来进行观察。这两个亚群的神经元都是γ-氨基丁酸能的。表达CP-AMPARs的神经元亚群中钙结合蛋白阳性神经元的比例（39.4±6.0%）高于表达CP-KARs的神经元亚群（CB神经元的14.2±7.5%）。此外，我们首次表明，NHCl诱导的去极化在表达CP-KARs和CP-AMPARs的γ-氨基丁酸能神经元中比在大多数谷氨酸能神经元中更快地诱导[Ca]升高。CP-AMPARs拮抗剂NASPM增加了在表达CP-KARs的γ-氨基丁酸能神经元中DoA诱导的Ca反应的幅度，表明表达CP-AMPARs的神经元支配表达CP-KARs的γ-氨基丁酸能神经元。我们推测抑制性神经元中的CP-KARs参与了过度兴奋时GABA释放超前的机制。
