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Review
. 2010 Feb 24;30(8):2807-9.
doi: 10.1523/JNEUROSCI.5984-09.2010.

CaMKK-CaMKI signaling pathways differentially control axon and dendrite elongation in cortical neurons

April P Neal  1 , Elizabeth Molina-Campos, Brenda Marrero-Rosado, Aaron B Bradford, Sara M Fox, Natalia Kovalova, Heidi E Hannon
Affiliations
Review

CaMKK-CaMKI signaling pathways differentially control axon and dendrite elongation in cortical neurons

April P Neal et al. J Neurosci. .
No abstract available

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Figures

Figure 1.
Figure 1.
CaMKK–CaMKI signaling in developing cortical neurons. Immature cortical neurons lack KCC2, a key transporter that normally causes chloride influx and thus hyperpolarization upon GABAA receptor (GABAAR) activation (Rivera et al., 1999). As a result, GABAAR activation in immature neurons causes depolarization and subsequent activation of voltage-gated Ca2+ channels (VGCC) and Ca2+ influx. Ca2+ binds calmodulin (CaM), allowing CaM to bind both CaMKK and CaMKI. Binding of CaM to CaMKI results in a conformational change in the activation loop, allowing phosphorylation by CaM-CaMKK and subsequent enzymatic activation (Wayman et al., 2008). CaMKIα activation results in axon outgrowth, while BDNF signaling in dendrites results in a rise of intracellular Ca2+, which cumulates in activation of CaMKIγ and dendrite outgrowth. This scheme incorporates combined results from Takemoto-Kimura et al. (2007) and Ageta-Ishihara et al. (2009).
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