Acid-Sensing Ion Channel 1a Contributes to the Prefrontal Cortex Ischemia-Enhanced Neuronal Activities in the Amygdala

被引:4
作者
Park, Gyeongah [1 ]
Ge, Qian [1 ]
Jin, Zhen [1 ]
Du, Jianyang [1 ,2 ]
机构
[1] Univ Tennessee, Hlth Sci Ctr, Dept Anat & Neurobiol, Memphis, TN 38163 USA
[2] Univ Tennessee, Hlth Sci Ctr, Neurosci Inst, Memphis, TN 38163 USA
关键词
cerebral ischemia; stroke; oxygen-glucose deprivation; acid-sensing ion channels; ASIC1a; prefrontal cortex; amygdala; brain circuits; endothelin-1; depression-like behaviors; synaptic transmission and plasticity; long-term potentiation; PLASTICITY; PH; RECOVERY; CALCIUM; FEAR;
D O I
10.3390/brainsci13121684
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Following a stroke, the emergence of amygdala-related disorders poses a significant challenge, with severe implications for post-stroke mental health, including conditions such as anxiety and depression. These disorders not only hinder post-stroke recovery but also elevate mortality rates. Despite their profound impact, the precise origins of aberrant amygdala function after a stroke remain elusive. As a target of reduced brain pH in ischemia, acid-sensing ion channels (ASICs) have been implicated in synaptic transmission after ischemia, hinting at their potential role in reshaping neural circuits following a stroke. This study delves into the intriguing relationship between post-stroke alterations and ASICs, specifically focusing on postsynaptic ASIC1a enhancement in the amygdala following prefrontal cortex (PFC) ischemia induced by endothelin-1 (ET-1) injection. Our findings intriguingly illustrate that mPFC ischemia not only accentuates the PFC to the amygdala circuit but also implicates ASIC1a in fostering augmented synaptic plasticity after ischemia. In contrast, the absence of ASIC1a impairs the heightened induction of long-term potentiation (LTP) in the amygdala induced by ischemia. This pivotal research introduces a novel concept with the potential to inaugurate an entirely new avenue of inquiry, thereby significantly enhancing our comprehension of the intricate mechanisms underlying post-stroke neural circuit reconfiguration. Importantly, these revelations hold the promise of paving the way for groundbreaking therapeutic interventions.
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页数:14
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