Excitatory transmission onto AgRP neurons is regulated by cJun NH2-terminal kinase 3 in response to metabolic stress

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Excitatory transmission onto AgRP neurons is regulated by cJun NH2-terminal kinase 3 in response to metabolic stress

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Title: Excitatory transmission onto AgRP neurons is regulated by cJun NH2-terminal kinase 3 in response to metabolic stress
Author: Vernia, Santiago; Morel, Caroline; Madara, Joseph C; Cavanagh-Kyros, Julie; Barrett, Tamera; Chase, Kathryn; Kennedy, Norman J; Jung, Dae Young; Kim, Jason K; Aronin, Neil; Flavell, Richard A; Lowell, Bradford B; Davis, Roger J

Note: Order does not necessarily reflect citation order of authors.

Citation: Vernia, S., C. Morel, J. C. Madara, J. Cavanagh-Kyros, T. Barrett, K. Chase, N. J. Kennedy, et al. 2016. “Excitatory transmission onto AgRP neurons is regulated by cJun NH2-terminal kinase 3 in response to metabolic stress.” eLife 5 (1): e10031. doi:10.7554/eLife.10031. http://dx.doi.org/10.7554/eLife.10031.
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Abstract: The cJun NH2-terminal kinase (JNK) signaling pathway is implicated in the response to metabolic stress. Indeed, it is established that the ubiquitously expressed JNK1 and JNK2 isoforms regulate energy expenditure and insulin resistance. However, the role of the neuron-specific isoform JNK3 is unclear. Here we demonstrate that JNK3 deficiency causes hyperphagia selectively in high fat diet (HFD)-fed mice. JNK3 deficiency in neurons that express the leptin receptor LEPRb was sufficient to cause HFD-dependent hyperphagia. Studies of sub-groups of leptin-responsive neurons demonstrated that JNK3 deficiency in AgRP neurons, but not POMC neurons, was sufficient to cause the hyperphagic response. These effects of JNK3 deficiency were associated with enhanced excitatory signaling by AgRP neurons in HFD-fed mice. JNK3 therefore provides a mechanism that contributes to homeostatic regulation of energy balance in response to metabolic stress. DOI: http://dx.doi.org/10.7554/eLife.10031.001
Published Version: doi:10.7554/eLife.10031
Other Sources: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4798947/pdf/
Terms of Use: This article is made available under the terms and conditions applicable to Other Posted Material, as set forth at http://nrs.harvard.edu/urn-3:HUL.InstRepos:dash.current.terms-of-use#LAA
Citable link to this page: http://nrs.harvard.edu/urn-3:HUL.InstRepos:26318539
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