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Requirement of dendritic calcium spikes for induction of spike‐timing‐dependent synaptic plasticity
Author(s) -
Kampa Björn M.,
Letzkus Johannes J.,
Stuart Greg J.
Publication year - 2006
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jphysiol.2006.111062
Subject(s) - long term potentiation , excitatory postsynaptic potential , neuroscience , nmda receptor , postsynaptic potential , synaptic plasticity , post tetanic potentiation , nonsynaptic plasticity , ltp induction , spike timing dependent plasticity , pairing , chemistry , biophysics , biology , inhibitory postsynaptic potential , physics , metaplasticity , receptor , biochemistry , superconductivity , quantum mechanics
Spike‐timing‐dependent synaptic plasticity (STDP) by definition requires the temporal association of pre‐ and postsynaptic action potentials (APs). Yet, in cortical pyramidal neurons pairing unitary EPSPs with single APs at low frequencies is ineffective at generating plasticity. Using recordings from synaptically coupled layer 5 pyramidal neurons, we show here that high‐frequency (200 Hz) postsynaptic AP bursts, rather than single APs, are required for both long‐term potentiation (LTP) induction and NMDA channel activation during EPSP–AP pairing at low frequencies. Furthermore, we find that AP bursts can lead to LTP induction and NMDA channel activation during EPSP–AP pairing at both positive and negative times. High‐frequency AP bursts generated supralinear calcium signals in basal dendrites suggesting the generation of dendritic calcium spikes, as has been observed previously in apical dendrites during AP burst firing at frequencies greater than 100 Hz. Consistent with a role of these dendritic calcium spikes in LTP induction, pairing EPSPs with low frequency (50 Hz) AP bursts was ineffective in generating LTP. Furthermore, supralinear calcium signals in basal dendrites during AP bursts were blocked by low concentrations of the T‐ and R‐type calcium channel antagonist nickel, which also blocked LTP and NMDA channel activation. These data suggest an important role of dendritic calcium spikes during AP bursts in determining both the efficacy and time window for STDP induction.