한빛사 논문
Pojeong Park1,2,3,4, John Georgiou3, Thomas M. Sanderson1,2,3, Kwang-Hee Ko2, Heather Kang1,2,3,4, Ji-il Kim2, Clarrisa A. Bradley2,5, Zuner A. Bortolotto1, Min Zhuo2,4, Bong-Kiun Kaang2 & Graham L. Collingridge1,2,3,4,6,*
1Glutamate Receptor Group, School of Physiology, Pharmacology and Neuroscience, University of Bristol, Bristol, United Kingdom.
2Department of Biological Sciences, College of Natural Sciences, Seoul National University, Seoul 08826, Korea.
3Lunenfeld-Tanenbaum Research Institute, Mount Sinai Hospital, Toronto, ON M5G 1X5, Canada.
4Department of Physiology, University of Toronto, Toronto, ON M5S 1A8, Canada. 5Neurosciences and Mental Health, Peter Gilgan Centre for Research and Learning, The Hospital for Sick Children, Toronto, ON M5G 0A4, Canada.
6TANZ Centre for Research in Neurodegenerative Diseases, University of Toronto, Toronto, ON M5S 1A8, Canada.
*Corresponding author
Abstract
Long-term potentiation (LTP) at hippocampal CA1 synapses can be expressed by an increase either in the number (N) of AMPA (α-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid) receptors or in their single channel conductance (γ). Here, we have established how these distinct synaptic processes contribute to the expression of LTP in hippocampal slices obtained from young adult rodents. LTP induced by compressed theta burst stimulation (TBS), with a 10 s inter-episode interval, involves purely an increase in N (LTPN). In contrast, either a spaced TBS, with a 10 min inter-episode interval, or a single TBS, delivered when PKA is activated, results in LTP that is associated with a transient increase in γ (LTPγ), caused by the insertion of calcium-permeable (CP)-AMPA receptors. Activation of CaMKII is necessary and sufficient for LTPN whilst PKA is additionally required for LTPγ. Thus, two mechanistically distinct forms of LTP co-exist at these synapses.
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