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Heterosynaptic metaplastic regulation of synaptic efficacy in CA1 pyramidal neurons of rat hippocampus
Author(s) -
Le Ray Didier,
Fernández De Sevilla David,
Belén Porto Ana,
Fuenzalida Marco,
Buño Washington
Publication year - 2004
Publication title -
hippocampus
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.767
H-Index - 155
eISSN - 1098-1063
pISSN - 1050-9631
DOI - 10.1002/hipo.20021
Subject(s) - metaplasticity , long term potentiation , neuroscience , synaptic plasticity , hippocampus , nonsynaptic plasticity , ltp induction , synaptic augmentation , synaptic fatigue , excitatory postsynaptic potential , chemistry , biology , inhibitory postsynaptic potential , receptor , biochemistry
The induction threshold, and the magnitude and direction of changes in synaptic plasticity may depend on the previous history of neuronal activity. This phenomenon, termed “metaplasticity,” could play an important role in integration processes by coordinating the modulation of synapses. Although metaplasticity has been analyzed extensively, its underlying cellular mechanisms remain largely unknown. Using in vitro electrophysiological and computer simulation approaches, we investigated the contribution of the slow Ca 2+ ‐dependent afterhyperpolarization (sAHP) in the metaplastic control of the induction of long‐term potentiation (LTP) at convergent CA3‐CA1 pyramidal neuron synapses. We report that classical conditioning protocols may lead to the simultaneous induction of a sustained homosynaptic LTP and a potentiation of the sAHP that endured ≈1 h. The sAHP potentiation dramatically altered the spike responses of the CA1 pyramidal neuron. Of particular interest was the reduction of the CA1 neuron excitability and, consequently, of the capacity of a nonpotentiated synaptic input to elicit spikes while the sAHP was potentiated. This reduction in excitability temporarily prevented nonpotentiated synaptic inputs to exhibit an LTP induced by presynaptic tetanization. This metaplasticity was strongly resistant to increases in the magnitude of synaptic tetanization protocols. We propose that this heterosynaptic metaplasticity, mediated by intrinsic cellular mechanisms, triggered by brief periods of activity, and relying on changes of a slow Ca 2+ ‐activated K + current, may contribute to adjusting the efficacy of synaptic connections and shaping network behavior to regulate integration processes. © 2004 Wiley‐Liss, Inc.