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                  <date type="datePub">2014-03-25</date>
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              <p>Cognitive and behavioral disorders are thought to be a result of neuronal dysfunction, but the underlying molecular defectsremain 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 associatedwith neurobehavioral dysfunction, in the modulation of cyclic AMP/PKA signaling. We found that coronin 1 is specificallyexpressed in excitatory but not inhibitory neurons and that coronin 1 deficiency results in loss of excitatory synapses andsevere 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 forcyclic–AMP–protein kinase A–dependent presynaptic plasticity. We further show that upon cell surface stimulation, coronin1 interacted with the G protein subtype Gas to stimulate the cAMP/PKA pathway. The absence of coronin 1 or expression ofcoronin 1 mutants unable to interact with Gas resulted in a marked reduction in cAMP signaling. Strikingly, synapticplasticity and behavioral defects of coronin 1–deficient mice were restored by in vivo infusion of a membrane-permeablecAMP analogue. Together these results identify coronin 1 as being important for cognition and behavior through its activityin promoting cAMP/PKA-dependent synaptic plasticity and may open novel avenues for the dissection of signaltransduction pathways involved in neurobehavioral processes</p>
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