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© Shalin E. Abraham, Michael Häusser, Christoph Schmidt-Hieber, University College London
The dentate gyrus is one of the few mammalian brain regions where new neurons are generated throughout life. The image was taken with a confocal microscope from a parasagittal slice of the mouse hippocampus. Cells were labelled with fluorescent markers: Newly generated neurons are red (doublecortin), mature neurons are green (NeuN), and nuclei are blue (DAPI)
Publication : PLoS biology

Coronin 1 regulates cognition and behavior through modulation of cAMP/protein kinase A signaling

Scientific Fields
Diseases
Organisms
Applications
Technique

Published in PLoS biology - 25 Mar 2014

Jayachandran R*, Liu X*, Bosedasgupta S*, Müller P*, Zhang CL, Moshous D, Studer V, Schneider J, Genoud C, Fossoud C, Gambino F, Khelfaoui M, Müller C, Bartholdi D, Rossez H, Stiess M, Houbaert X, Jaussi R, Frey D, Kammerer RA, Deupi X, de Villartay JP, Lüthi A, Humeau Y, Pieters J

Link to Pubmed [PMID] – 24667537

PLoS Biol. 2014 Mar;12(3):e1001820

Cognitive and behavioral disorders are thought to be a result of neuronal dysfunction, but the underlying molecular defects remain largely unknown. An important signaling pathway involved in the regulation of neuronal function is the cyclic AMP/Protein kinase A pathway. We here show an essential role for coronin 1, which is encoded in a genomic region associated with neurobehavioral dysfunction, in the modulation of cyclic AMP/PKA signaling. We found that coronin 1 is specifically expressed in excitatory but not inhibitory neurons and that coronin 1 deficiency results in loss of excitatory synapses and severe neurobehavioral disabilities, including reduced anxiety, social deficits, increased aggression, and learning defects. Electrophysiological analysis of excitatory synaptic transmission in amygdala revealed that coronin 1 was essential for cyclic-AMP-protein kinase A-dependent presynaptic plasticity. We further show that upon cell surface stimulation, coronin 1 interacted with the G protein subtype Gαs to stimulate the cAMP/PKA pathway. The absence of coronin 1 or expression of coronin 1 mutants unable to interact with Gαs resulted in a marked reduction in cAMP signaling. Strikingly, synaptic plasticity and behavioral defects of coronin 1-deficient mice were restored by in vivo infusion of a membrane-permeable cAMP analogue. Together these results identify coronin 1 as being important for cognition and behavior through its activity in promoting cAMP/PKA-dependent synaptic plasticity and may open novel avenues for the dissection of signal transduction pathways involved in neurobehavioral processes.

https://www.ncbi.nlm.nih.gov/pubmed/24667537