Laboratory of Molecular Basis of Behavior, the Nencki Institute of Experimental Biology of Polish Academy of Sciences, Warsaw, Poland.
Department Molecular Neuropharmacology, Maj Institute of Pharmacology of Polish Academy of Sciences, Krakow, Poland.
PLoS Biol. 2023 May 8;21(5):e3002106. doi: 10.1371/journal.pbio.3002106. eCollection 2023 May.
The updating of contextual memories is essential for survival in a changing environment. Accumulating data indicate that the dorsal CA1 area (dCA1) contributes to this process. However, the cellular and molecular mechanisms of contextual fear memory updating remain poorly understood. Postsynaptic density protein 95 (PSD-95) regulates the structure and function of glutamatergic synapses. Here, using dCA1-targeted genetic manipulations in vivo, combined with ex vivo 3D electron microscopy and electrophysiology, we identify a novel, synaptic mechanism that is induced during attenuation of contextual fear memories and involves phosphorylation of PSD-95 at Serine 73 in dCA1. Our data provide the proof that PSD-95-dependent synaptic plasticity in dCA1 is required for updating of contextual fear memory.
更新情境记忆对于在不断变化的环境中生存至关重要。越来越多的数据表明，背侧 CA1 区（dCA1）有助于这一过程。然而，情境恐惧记忆更新的细胞和分子机制仍知之甚少。突触后密度蛋白 95（PSD-95）调节谷氨酸能突触的结构和功能。在这里，我们通过体内靶向 dCA1 的基因操作，结合离体 3D 电子显微镜和电生理学，鉴定出一种在情境恐惧记忆衰减过程中诱导的新型突触机制，该机制涉及 dCA1 中 PSD-95 的丝氨酸 73 磷酸化。我们的数据提供了证据，表明 dCA1 中 PSD-95 依赖性突触可塑性是更新情境恐惧记忆所必需的。
