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• W4283463851 abstract "Abstract Learning, memory and cognition are thought to require forms of synaptic plasticity such as hippocampal long-term potentiation and depression (LTP and LTD), and such plasticity can be modulated by β-adrenergic stimulation with isoproterenol or norepinephrine. For instance, LTP versus LTD is induced by high-versus low-frequency stimulation (HFS versus LFS) but, stimulating β-adrenergic receptors (βARs) enables LTP induction also by LFS. In contrast to HFS-LTP, such βAR-LTP requires signaling by L-type voltage-gated Ca 2+ -channels, not NMDA-type glutamate receptors (NMDARs). Surprisingly, we found that βAR-LTP still required a non-ionotropic NMDAR function: the stimulus-induced binding of the Ca 2+ /calmodulin-dependent protein kinase II (CaMKII) that mediates CaMKII movement to excitatory synapses. In hippocampal neurons, β-adrenergic stimulation with isoproterenol transformed LTD-type CaMKII movement to LTP-type movement, resulting in CaMKII movement to excitatory instead of inhibitory synapses. Additionally, isoproterenol enabled induction of a major cell-biological feature of LTP in response to LTD stimuli: increased SEP-GluA1 surface expression. Like for the βAR-LTP in hippocampal slices, the effects of isoproterenol on CaMKII movement and SEP-GluA1 surface expression involved L-type Ca 2+ -channels. Taken together, these results indicate that isoproterenol transforms LTD stimuli to LTP signals by switching CaMKII movement and GluN2B binding to LTP mode. One Sentence Summary Buonarati et al. show that β-adrenergic stimulation enables LTP induction in response to LTD stimuli by switching synaptic CaMKII movement to LTP mode." @default.
• W4283463851 created "2022-06-26" @default.
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• W4283463851 date "2022-06-24" @default.
• W4283463851 modified "2023-09-28" @default.
• W4283463851 title "CaMKII binding to GluN2B flips a β-adrenergic switch from synaptic depression to potentiation" @default.
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• W4283463851 doi "https://doi.org/10.1101/2022.06.23.497296" @default.
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