GABA Regulation of Burst Firing in Hippocampal Astrocyte Neural Circuit: A Biophysical Model
GABA Regulation of Burst Firing in Hippocampal Astrocyte Neural Circuit: A Biophysical Model
复制标题
DOI：
10.3389/fncel.2019.00335
复制
发表时间：
2019-07-23
影响因子：
5.3
通讯作者：
Halliday, David M.
中科院分区：
文献类型：
--
作者：
Liu, Junxiu;McDaid, Liam;Halliday, David M.
目前广泛认为，神经胶质细胞和γ-氨基丁酸能（GABA）中间神经元在时间和空间上动态调节突触传递和神经元活动。本文提出了一个生物物理模型，捕捉星形胶质细胞，GABA中间神经元和前/突触后神经元之间的相互作用。具体地，从GABA中间神经元释放的GABA在星形胶质细胞中触发钙（Ca 2+）经由肌醇1，4，5-三磷酸（IP 3）途径从内质网释放。这导致神经胶质传递，其提高突触前传递概率率（PR），引起重量增强和突触后神经元放电的逐渐增加，最终稳定。然而，通过捕获的IP 3之间的复杂的相互作用，产生的GABA和2-花生四烯酸甘油（2-AG）的途径，和PR，本文表明，这种相互作用不仅引起了一个初始的重量增强阶段，但这一阶段之后是突触后爆发行为。此外，该模型将表明，有一个突触前的频率范围内，爆发式放电可以发生。所提出的模型提供了一种新的细胞水平机制，可以支持神经元样活动和不同脑区的神经元同步。
It is now widely accepted that glia cells and gamma-aminobutyric acidergic (GABA) interneurons dynamically regulate synaptic transmission and neuronal activity in time and space. This paper presents a biophysical model that captures the interaction between an astrocyte cell, a GABA interneuron and pre/postsynaptic neurons. Specifically, GABA released from a GABA interneuron triggers in astrocytes the release of calcium (Ca2+) from the endoplasmic reticulum via the inositol 1, 4, 5-trisphosphate (IP3) pathway. This results in gliotransmission which elevates the presynaptic transmission probability rate (PR) causing weight potentiation and a gradual increase in postsynaptic neuronal firing, that eventually stabilizes. However, by capturing the complex interactions between IP3, generated from both GABA and the 2-arachidonyl glycerol (2-AG) pathway, and PR, this paper shows that this interaction not only gives rise to an initial weight potentiation phase but also this phase is followed by postsynaptic bursting behavior. Moreover, the model will show that there is a presynaptic frequency range over which burst firing can occur. The proposed model offers a novel cellular level mechanism that may underpin both seizure-like activity and neuronal synchrony across different brain regions.