薬理学講座では、
生体内でのLTP様のシナプス変化を反映している可能性がある、CapZの再分布に着目しています。Arc-PromotorでEGFP-CapZを発現している安定なTGマウス AiCE-Tgを開発し、脳の、広い意味での可塑性を研究するツールと考え、記憶という生理現象や関連病理の解析の糸口、と期待して研究展開しています。

Abstract Sneak peak　
The F-actin capping protein CapZ accumulates preferentially in dendritic spines within regions exposed to long-term potentiation (LTP)-inducing stimuli. To develop an in vivo marker of synaptic plasticity, we generated a transgenic mouse line, AiCE-Tg, in which enhanced green fluorescent protein-tagged CapZ (EGFP-CapZ) is expressed in a subset of dendritic spines. Following unilateral visual or somatosensory stimulation, EGFP-CapZ signals were significantly enhanced in specific dendritic spines within the stimulated cortex, with this effect abolished by NMDA receptor blockade. Immunolabeling for α-actinin—a PSD-95–interacting protein known to recruit AMPA receptors—revealed that α-actinin was more frequently localized to the brightest EGFP-CapZ–positive spines (top 100) than to less bright ones (top 1000). These input-dependent changes in EGFP-CapZ distribution likely reflect LTP-like synaptic modifications in vivo and suggest that EGFP-CapZ may serve as a molecular tool for investigating synaptic plasticity.

References　SciRep2020　JEM2022 (日本語での説明文はこちらをクリック)

Fig. 3G in JEM 2022 shows the absence of “eat me signal”; PS on EGFP-CapZ positive (~Active？) spines in the AiCE-Tg mice.
© 2022 Kurematsu et al. Originally published in Journal of Experimental Medicine

Email：　makiky@kph.bunri-u.ac.jp / makiky-tky@umin.ac.jp