Journal
JOURNAL OF NEUROSCIENCE
Volume 36, Issue 2, Pages 622-631Publisher
SOC NEUROSCIENCE
DOI: 10.1523/JNEUROSCI.3625-15.2016
Keywords
calcium-permeable AMPA receptor; hippocampus; long-term potentiation; NMDA receptor; PKA; rectification
Categories
Funding
- Medical Research Council
- ERC [RD1819, R08898]
- Canadian lnstitute for Health Research (CIFIR) Michael Smith Chair in Neurosciences and Mental Health
- Canada Research Chair
- CIHR Operating Grant [MOP-124807]
- Natural Sciences and Engineering Research Council of Canada [RGPIN 402555]
- Azrieli Neurodevelopmental Research Program and Brain Canada
- National Honor Scientist Program of the National Research Foundation - Korea government
- Biotechnology and Biological Sciences Research Council [BB/K019899/1] Funding Source: researchfish
- Medical Research Council [MR/K023098/1] Funding Source: researchfish
- BBSRC [BB/K019899/1] Funding Source: UKRI
- MRC [MR/K023098/1] Funding Source: UKRI
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Two forms of NM DA receptor (NMDAR)-dependent long-term potentiation (LIP) at hippocampal CAI synapses can be distinguished based on their sensitivity to inhibitors of protein kinase A (PKA). The PKA-dependent form requires multiple episodes of high-frequency stimulation (HFS) or theta burst stimuli (TBS) with a spacing between episodes in the order of minutes. To investigate the mechanism by which spaced episodes induce the PKA-dependent form of LIP, we have compared, in interleaved experiments, spaced (s) and compressed (c) TBS protocols in the rat CAI synapses. We find that LIP induced by sTBS, but not that induced by cTBS, involves the insertion of calcium-permeable (CP) AMPARs, as assessed using pharmacological and electrophysiological criteria. Furthermore, a single TBS when paired with rolipram [4-(3-(cyclopentyloxy)-4-methoxyphenyl)pyrrolidin-2-one], to activate PKA, generates an LTP that also involves the insertion of CP-AMPARs. These data demonstrate that the involvement of CP-AMPARs in LTP is critically determined by the timing of the induction trigger and is associated specifically with the PKA-dependent form of LIP.
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