Age‐related impairment of declarative memory: linking memorization of temporal associations to GluN2B redistribution in dorsal CA1,Aging Cell

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Age‐related impairment of declarative memory: linking memorization of temporal associations to GluN2B redistribution in dorsal CA1
Aging Cell ( IF 8.0 ) Pub Date : 2020-10-03 , DOI: 10.1111/acel.13243
Alice Shaam Al Abed _{1,

2,

3} , Azza Sellami _{1,

2} , Mylene Potier _{1,

3} , Eva-Gunnel Ducourneau _{1,

2} , Pauline Gerbeaud-Lassau _{1,

2} , Laurent Brayda-Bruno _{1,

2} , Valerie Lamothe _{1,

3} , Nathalie Sans _{1,

2} , Aline Desmedt _{1,

2} , Peter Vanhoutte _{4,

5,

6} , Catherine Bennetau-Pelissero _{1,

3} , Pierre Trifilieff ₇ , Aline Marighetto _{1,

2}

Affiliation

GluN2B subunits of NMDA receptors have been proposed as a target for treating age‐related memory decline. They are indeed considered as crucial for hippocampal synaptic plasticity and hippocampus‐dependent memory formation, which are both altered in aging. Because a synaptic enrichment in GluN2B is associated with hippocampal LTP in vitro, a similar mechanism is expected to occur during memory formation. We show instead that a reduction of GluN2B synaptic localization induced by a single‐session learning in dorsal CA1 apical dendrites is predictive of efficient memorization of a temporal association. Furthermore, synaptic accumulation of GluN2B, rather than insufficient synaptic localization of these subunits, is causally involved in the age‐related impairment of memory. These challenging data identify extra‐synaptic redistribution of GluN2B‐containing NMDAR induced by learning as a molecular signature of memory formation and indicate that modulating GluN2B synaptic localization might represent a useful therapeutic strategy in cognitive aging.

中文翻译：

年龄相关的陈述性记忆损伤：将时间关联的记忆与背侧 CA1 中的 GluN2B 重新分布联系起来

NMDA 受体的 GluN2B 亚基已被提议作为治疗与年龄相关的记忆衰退的靶标。它们确实被认为对海马突触可塑性和海马依赖性记忆形成至关重要，而这两者都会随着衰老而改变。由于 GluN2B 突触富集与体外海马 LTP 相关，因此预计在记忆形成过程中也会发生类似的机制。相反，我们表明，背侧 CA1 顶端树突的单次学习引起的 GluN2B 突触定位的减少可以预测时间关联的有效记忆。此外，GluN2B 的突触积累，而不是这些亚基的突触定位不足，与年龄相关的记忆障碍有关。这些具有挑战性的数据将学习诱导的含有 GluN2B 的 NMDAR 突触外重新分布确定为记忆形成的分子特征，并表明调节 GluN2B 突触定位可能代表了认知衰老的一种有用的治疗策略。

更新日期：2020-10-23

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