Genetically Increased Cell-Intrinsic Excitability Enhances Neuronal Integration into Adult Brain Circuits
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Lin-2010-Genetically Increase.pdf
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Author(s)
Lin, Chia-Wei
Sim, Shuyin
Ainsworth, Alice
Okada, Masayoshi
Kelsch, Wolfgang
Lois, Carlos
Date Issued
January 2010
Journal
Neuron
Publisher
Elsevier
Citation
Lin, Chia-Wei, Shuyin Sim, Alice Ainsworth, Masayoshi Okada, Wolfgang Kelsch, and Carlos Lois. “Genetically Increased Cell-Intrinsic Excitability Enhances Neuronal Integration into Adult Brain Circuits.” Neuron 65, no. 1 (January 2010): 32–39. © 2010 Elsevier Inc.
Version
Final published version
Abstract
New neurons are added to the adult brain throughout life, but only half ultimately integrate into existing circuits. Sensory experience is an important regulator of the selection of new neurons but it remains unknown whether experience provides specific patterns of synaptic input or simply a minimum level of overall membrane depolarization critical for integration. To investigate this issue, we genetically modified intrinsic electrical properties of adult-generated neurons in the mammalian olfactory bulb. First, we observed that suppressing levels of cell-intrinsic neuronal activity via expression of ESKir2.1 potassium channels decreases, whereas enhancing activity via expression of NaChBac sodium channels increases survival of new neurons. Neither of these modulations affects synaptic formation. Furthermore, even when neurons are induced to fire dramatically altered patterns of action potentials, increased levels of cell-intrinsic activity completely blocks cell death triggered by NMDA receptor deletion. These findings demonstrate that overall levels of cell-intrinsic activity govern survival of new neurons and precise firing patterns are not essential for neuronal integration into existing brain circuits.
MIT Department
Massachusetts Institute of Technology. Department of Brain and Cognitive Sciences
Picower Institute for Learning and Memory
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Article is made available in accordance with the publisher's policy and may be subject to US copyright law. Please refer to the publisher's site for terms of use.
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DOI of Published Version
https://doi.org/10.1016/j.neuron.2009.12.001
