| First Author | Xiao K | Year | 2023 |
| Journal | Sci Adv | Volume | 9 |
| Issue | 36 | Pages | eadi3088 |
| PubMed ID | 37672577 | Mgi Jnum | J:340572 |
| Mgi Id | MGI:7528104 | Doi | 10.1126/sciadv.adi3088 |
| Citation | Xiao K, et al. (2023) A critical role for CaMKII in behavioral timescale synaptic plasticity in hippocampal CA1 pyramidal neurons. Sci Adv 9(36):eadi3088 |
| abstractText | Behavioral timescale synaptic plasticity (BTSP) is a type of non-Hebbian synaptic plasticity reported to underlie place field formation. Despite this important function, the molecular mechanisms underlying BTSP are poorly understood. The alpha-calcium-calmodulin-dependent protein kinase II (alphaCaMKII) is activated by synaptic transmission-mediated calcium influx, and its subsequent phosphorylation is central to synaptic plasticity. Because the activity of alphaCaMKII is known to outlast the event triggering phosphorylation, we hypothesized that it could mediate the extended timescale of BTSP. To examine the role of alphaCaMKII in BTSP, we performed whole-cell in vivo and in vitro recordings in CA1 pyramidal neurons from mice engineered with a point mutation at the autophosphorylation site (T286A) causing accelerated signaling kinetics. Here, we demonstrate a profound deficit in synaptic plasticity, strongly suggesting that alphaCaMKII signaling is required for BTSP. This study elucidates part of the molecular mechanism of BTSP and provides insight into the function of alphaCaMKII in place cell formation and ultimately learning and memory. |
