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Hippocampus. 2011 Mar;21(3):288-97. doi: 10.1002/hipo.20748.

Dendritic mechanisms controlling the threshold and timing requirement of synaptic plasticity.

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Department of Neuroscience, University of Minnesota, Minneapolis, USA.


Active conductances located and operating on neuronal dendrites are expected to regulate synaptic integration and plasticity. We investigate how Kv4.2-mediated A-type K(+) channels and Ca(2+) -activated K(+) channels are involved in the induction process of Hebbian-type plasticity that requires correlated pre- and postsynaptic activities. In CA1 pyramidal neurons, robust long-term potentiation (LTP) induced by a theta burst pairing protocol usually occurred within a narrow window during which incoming synaptic potentials coincided with postsynaptic depolarization. Elimination of dendritic A-type K(+) currents in Kv4.2(-/-) mice, however, resulted in an expanded time window, making the induction of synaptic potentiation less dependent on the temporal relation of pre- and postsynaptic activity. For the other type of synaptic plasticity, long-term depression, the threshold was significantly increased in Kv4.2(-/-) mice. This shift in depression threshold was restored to normal when the appropriate amount of internal free calcium was chelated during induction. In concert with A-type channels, Ca(2+) -activated K(+) channels also exerted a sliding effect on synaptic plasticity. Blocking these channels in Kv4.2(-/-) mice resulted in an even larger potentiation while by contrast, the depression threshold was shifted further. In conclusion, dendritic A-type and Ca(2+) -activated K(+) channels dually regulate the timing-dependence and thresholds of synaptic plasticity in an additive way.

[Indexed for MEDLINE]

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