Institute of Physiology, University Medical Center of the Johannes Gutenberg University, Mainz, Germany.
PLoS Comput Biol. 2021 Nov 12;17(11):e1009199. doi: 10.1371/journal.pcbi.1009199. eCollection 2021 Nov.
GABA (γ-amino butyric acid) is an inhibitory neurotransmitter in the adult brain that can mediate depolarizing responses during development or after neuropathological insults. Under which conditions GABAergic membrane depolarizations are sufficient to impose excitatory effects is hard to predict, as shunting inhibition and GABAergic effects on spatiotemporal filtering of excitatory inputs must be considered. To evaluate at which reversal potential a net excitatory effect was imposed by GABA (EGABAThr), we performed a detailed in-silico study using simple neuronal topologies and distinct spatiotemporal relations between GABAergic and glutamatergic inputs. These simulations revealed for GABAergic synapses located at the soma an EGABAThr close to action potential threshold (EAPThr), while with increasing dendritic distance EGABAThr shifted to positive values. The impact of GABA on AMPA-mediated inputs revealed a complex temporal and spatial dependency. EGABAThr depends on the temporal relation between GABA and AMPA inputs, with a striking negative shift in EGABAThr for AMPA inputs appearing after the GABA input. The spatial dependency between GABA and AMPA inputs revealed a complex profile, with EGABAThr being shifted to values negative to EAPThr for AMPA synapses located proximally to the GABA input, while for distally located AMPA synapses the dendritic distance had only a minor effect on EGABAThr. For tonic GABAergic conductances EGABAThr was negative to EAPThr over a wide range of gGABAtonic values. In summary, these results demonstrate that for several physiologically relevant situations EGABAThr is negative to EAPThr, suggesting that depolarizing GABAergic responses can mediate excitatory effects even if EGABA did not reach EAPThr.
GABA(γ-氨基丁酸)是成人脑中的一种抑制性神经递质,它可以在发育过程中或神经病理损伤后介导去极化反应。在何种条件下 GABA 能膜去极化足以产生兴奋效应是很难预测的,因为需要考虑短路抑制和 GABA 对兴奋性输入的时空滤波的影响。为了评估 GABA(EGABAThr)引起净兴奋效应的反转电位,我们使用简单的神经元拓扑结构和 GABA 能和谷氨酸能输入之间的不同时空关系进行了详细的计算机模拟研究。这些模拟结果表明,位于神经元胞体的 GABA 能突触的 EGABAThr 接近动作电位阈值(EAPThr),而随着树突距离的增加,EGABAThr 向正值移动。GABA 对 AMPA 介导的输入的影响揭示了一种复杂的时间和空间依赖性。EGABAThr 取决于 GABA 和 AMPA 输入之间的时间关系,对于 GABA 输入之后出现的 AMPA 输入,EGABAThr 有明显的负向偏移。GABA 和 AMPA 输入之间的空间依赖性揭示了一种复杂的分布,对于靠近 GABA 输入的 AMPA 突触,EGABAThr 向负值偏移,而对于位于远端的 AMPA 突触,树突距离对 EGABAThr 的影响较小。对于紧张性 GABA 能电导,EGABAThr 在很宽的 gGABAtonic 值范围内都低于 EAPThr。总之,这些结果表明,对于几种生理相关的情况,EGABAThr 低于 EAPThr,表明去极化的 GABA 能反应即使 EGABA 未达到 EAPThr,也可以介导兴奋效应。