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<p>Maintaining GABAergic inhibition within physiological limits in the medial prefrontal cortex (mPFC) is critical for working memory. While synaptic GABA<sub>A</sub>R typically mediate the primary component of mPFC inhibition, the role of extrasynaptic δ-GABA<sub>A</sub>R in working memory remains unclear. To investigate this, we used fiber photometry to examine the effects of δ-GABA<sub>A</sub>R in freely moving mice. Our results indicate that the loss of δ-GABA<sub>A</sub>R expression leads to learning and memory impairment. Specifically, activation of δ-GABA<sub>A</sub>R impaired learning and memory in WT mice but enhanced learning and memory in δ<sup>+/−</sup> knockout mice. Furthermore, δ-GABA<sub>A</sub>R activation increased calcium activity in the mPFC pyramidal neurons, an effect not observed in δ-Cas9-sgRNA virus-infected mice. Collectively, these findings suggest that δ-GABA<sub>A</sub>R deficiency impairs learning and memory by modulating the excitability of pyramidal neurons in the mPFC. These results delineate the functional contribution of δ-GABA<sub>A</sub>R to learning and memory, suggesting their role extends beyond the mere maintenance of information.</p>

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Gene Deficiency of δ Subunit-Containing GABAA Receptor in mPFC Lead Learning and Memory Impairment in Mice

  • 期刊论文

  • 发表日期：

    2025年1月3日

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  • Lin Cong,
  • Tianshu Zhang,
  • Teng Zhang,
  • Yifan Liu,
  • Yunxiao Li,
  • Xiaogang Pang,
  • Lianbin Zhao,
  • Tongrui Wu,
  • Shengkai Ding,
  • Yanling Liu,
  • Hao Wu,
  • Hui Shen,
  • Yuanyuan Li

摘要

Maintaining GABAergic inhibition within physiological limits in the medial prefrontal cortex (mPFC) is critical for working memory. While synaptic GABAAR typically mediate the primary component of mPFC inhibition, the role of extrasynaptic δ-GABAAR in working memory remains unclear. To investigate this, we used fiber photometry to examine the effects of δ-GABAAR in freely moving mice. Our results indicate that the loss of δ-GABAAR expression leads to learning and memory impairment. Specifically, activation of δ-GABAAR impaired learning and memory in WT mice but enhanced learning and memory in δ+/− knockout mice. Furthermore, δ-GABAAR activation increased calcium activity in the mPFC pyramidal neurons, an effect not observed in δ-Cas9-sgRNA virus-infected mice. Collectively, these findings suggest that δ-GABAAR deficiency impairs learning and memory by modulating the excitability of pyramidal neurons in the mPFC. These results delineate the functional contribution of δ-GABAAR to learning and memory, suggesting their role extends beyond the mere maintenance of information.