The neuronal and synaptic dynamics underlying post-inhibitory rebound burst related to major depressive disorder in the lateral habenula neuron model.

IF 4.3 3区 材料科学 Q1 ENGINEERING, ELECTRICAL & ELECTRONIC
ACS Applied Electronic Materials Pub Date : 2024-06-01 Epub Date: 2023-04-05 DOI:10.1007/s11571-023-09960-0
Kaihua Ma, Huaguang Gu, Yanbing Jia
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引用次数: 0

Abstract

A burst behavior observed in the lateral habenula (LHb) neuron related to major depressive disorder has attracted much attention. The burst is induced from silence by the excitatory N-methyl-D-aspartate (NMDA) synapse or by the inhibitory stimulation, i.e., a post-inhibitory rebound (PIR) burst, which has not been explained clearly. In the present paper, the neuronal and synaptic dynamics for the PIR burst are acquired in a theoretical neuron model. At first, dynamic cooperations between the fast rise of inhibitory γ-aminobutyric acid (GABA) synapse, slow rise of NMDA synapse, and T-type calcium current to evoke the PIR burst are obtained. Similar to the inhibitory pulse stimulation, fast rising GABA current can reduce the membrane potential to a level low enough to de-inactivate the low threshold T-type calcium current to evoke a PIR spike, which can enhance the slow rising NMDA current activated at a time before or after the PIR spike. The NMDA current following the PIR spike exhibits slow decay to induce multiple spikes to form the PIR burst. Such results present a theoretical explanation and a candidate for the PIR burst in real LHb neurons. Then, the dynamical mechanism for the PIR spike mediated by the T-type calcium channel is obtained. At large conductance of T-type calcium channel, the resting state corresponds to a stable focus near Hopf bifurcation and exhibits an "uncommon" threshold curve with membrane potential much lower than the resting membrane potential. Inhibitory modulation induces membrane potential decreased to run across the threshold curve to evoke the PIR spike. At small conductance of the T-type calcium channel, a stable node appears and manifests a common threshold curve with higher membrane potential, resulting in non-PIR phenomenon. The results present the dynamic cooperations between neuronal dynamics and fast/slow dynamics of different synapses for the PIR burst observed in the LHb neuron, which is helpful for the modulations to major depressive disorder.

侧缰状神经元模型中与重性抑郁症相关的抑制后反弹爆发的神经元和突触动力学
在与重度抑郁症有关的外侧哈伯神经元(LHb)中观察到的一种爆发行为引起了广泛关注。这种突发性是由兴奋性 N-甲基-D-天冬氨酸(NMDA)突触或抑制性刺激从沉默中诱发的,即抑制后反弹(PIR)突发性,目前还没有明确的解释。本文在一个理论神经元模型中获得了 PIR 突发性的神经元和突触动态。首先,获得了抑制性γ-氨基丁酸(GABA)突触的快速上升、NMDA突触的缓慢上升和T型钙电流之间的动态合作,从而唤起PIR爆发。与抑制性脉冲刺激类似,快速上升的 GABA 电流可将膜电位降至足够低的水平,使低阈值 T 型钙电流失活,从而唤起 PIR 尖峰,这可增强在 PIR 尖峰之前或之后激活的缓慢上升的 NMDA 电流。PIR 尖峰之后的 NMDA 电流表现出缓慢衰减,从而诱发多个尖峰,形成 PIR 阵发。这些结果从理论上解释了真实 LHb 神经元中的 PIR 突发性,并提出了一种候选方案。随后,我们得到了由 T 型钙通道介导的 PIR 尖峰的动力学机制。在 T 型钙通道的大电导率下,静息态对应于霍普夫分叉附近的稳定焦点,并呈现出膜电位远低于静息膜电位的 "不常见 "阈值曲线。抑制性调节诱导膜电位下降,使其跨越阈值曲线,从而唤起 PIR 尖峰。在 T 型钙通道电导较小的情况下,会出现一个稳定的节点,并表现出一条膜电位较高的普通阈值曲线,从而产生非 PIR 现象。研究结果表明,在 LHb 神经元中观察到的 PIR 阵发是神经元动态和不同突触的快慢动态之间的动态合作,这有助于对重度抑郁障碍的调节。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
CiteScore
7.20
自引率
4.30%
发文量
567
期刊介绍: ACS Applied Electronic Materials is an interdisciplinary journal publishing original research covering all aspects of electronic materials. The journal is devoted to reports of new and original experimental and theoretical research of an applied nature that integrate knowledge in the areas of materials science, engineering, optics, physics, and chemistry into important applications of electronic materials. Sample research topics that span the journal's scope are inorganic, organic, ionic and polymeric materials with properties that include conducting, semiconducting, superconducting, insulating, dielectric, magnetic, optoelectronic, piezoelectric, ferroelectric and thermoelectric. Indexed/​Abstracted: Web of Science SCIE Scopus CAS INSPEC Portico
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