Excellence Program for Higher Education of Hungary(FIKP‐2018, A.A.)
Advanced EMBO Fellowship Grant EMBO(ALTF 493-2017)
(TKP2020-IKA-05)
The perception of and response to danger is critical for an individual's survival
and is encoded by subcortical neurocircuits. The amygdaloid complex is the primary
neuronal site that initiates bodily reactions upon external threat with local-circuit
interneurons scaling output to effector pathways. Here, we categorize central amygdala
neurons that express secretagogin (Scgn), a Ca2+-sensor protein, as a subset of protein
kinase Cδ (PKCδ)+ interneurons, likely "off cells." Chemogenetic inactivation of Scgn+/PKCδ+
cells augmented conditioned response to perceived danger in vivo. While Ca2+-sensor
proteins are typically implicated in shaping neurotransmitter release presynaptically,
Scgn instead localized to postsynaptic compartments. Characterizing its role in the
postsynapse, we found that Scgn regulates the cell-surface availability of NMDA receptor
2B subunits (GluN2B) with its genetic deletion leading to reduced cell membrane delivery
of GluN2B, at least in vitro. Conclusively, we describe a select cell population,
which gates danger avoidance behavior with secretagogin being both a selective marker
and regulatory protein in their excitatory postsynaptic machinery.
