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A mechanism for homeostatic plasticity

Nature Neuroscience volume 7, pages 691–692 (2004)Cite this article

Neurons adapt to sustained alterations in activity by changing their intrinsic excitability. A form of this plasticity in hippocampal pyramidal neurons involves calcineurin-dependent dispersion and change in gating of K+ channels, reducing the cell's excitability.

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Figure 1: Misonou et al.3 hypothesize that calcium entry through ionotropic glutamate (NMDA) receptors, voltage-dependent calcium channels (VCC) or intracellular calcium release activates calcineurin (PP2B), leading to the dephosphorylation and dispersal of Kv2.1 clusters in hippocampal pyramidal neurons.
Figure 2: The shift in the voltage dependence of Kv2.1 activation reported by Misonou et al.3 (left) leads to a clear suppression of repetitive spiking in a computer simulation of a pyramidal neuron (right).

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Authors and Affiliations

  1. Department of Physiology, Northwestern University, Chicago, 60611, Illinois, USA

    D James Surmeier

  2. Department of Anatomy and Neurobiology, University of Tennessee, Memphis, 38163, Tennessee, USA

    Robert Foehring

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  1. D James Surmeier
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  2. Robert Foehring
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Surmeier, D., Foehring, R. A mechanism for homeostatic plasticity. Nat Neurosci 7, 691–692 (2004). https://doi.org/10.1038/nn0704-691

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