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cAMP-dependent cell differentiation triggered by activated CRHR1 in hippocampal neuronal cells

MPG-Autoren
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Deussing,  Jan M.
RG Jan Deussing, Molecular Neurogenetics, Dept. Stress Neurobiology and Neurogenetics, Max Planck Institute of Psychiatry, Max Planck Society;

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s41598-017-02021-7.pdf
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Zitation

Inda, C., Bonfiglio, J. J., dos Santos Claro, P. A., Senin, S. A., Armando, N. G., Deussing, J. M., et al. (2017). cAMP-dependent cell differentiation triggered by activated CRHR1 in hippocampal neuronal cells. SCIENTIFIC REPORTS, 7: 1944. doi:10.1038/s41598-017-02021-7.


Zitierlink: https://hdl.handle.net/21.11116/0000-0001-8A2D-2
Zusammenfassung
Corticotropin-releasing hormone receptor 1 (CRHR1) activates the atypical soluble adenylyl cyclase (sAC) in addition to transmembrane adenylyl cyclases (tmACs). Both cAMP sources were shown to be required for the phosphorylation of ERK1/2 triggered by activated G protein coupled receptor (GPCR) CRHR1 in neuronal and neuroendocrine contexts. Here, we show that activated CRHR1 promotes growth arrest and neurite elongation in neuronal hippocampal cells (HT22-CRHR1 cells). By characterising CRHR1 signalling mechanisms involved in the neuritogenic effect, we demonstrate that neurite outgrowth in HT22-CRHR1 cells takes place by a sAC-dependent, ERK1/2-independent signalling cascade. Both tmACs and sAC are involved in corticotropin-releasing hormone (CRH)mediated CREB phosphorylation and c-fos induction, but only sAC-generated cAMP pools are critical for the neuritogenic effect of CRH, further highlighting the engagement of two sources of cAMP downstream of the activation of a GPCR, and reinforcing the notion that restricted cAMP microdomains may regulate independent cellular processes.