| First Author | Hevesi Z | Year | 2021 |
| Journal | Proc Natl Acad Sci U S A | Volume | 118 |
| Issue | 7 | PubMed ID | 33558223 |
| Mgi Jnum | J:302607 | Mgi Id | MGI:6508004 |
| Doi | 10.1073/pnas.1921123118 | Citation | Hevesi Z, et al. (2021) Secretagogin marks amygdaloid PKCdelta interneurons and modulates NMDA receptor availability. Proc Natl Acad Sci U S A 118(7):e1921123118 |
| abstractText | 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 Ca(2+)-sensor protein, as a subset of protein kinase Cdelta (PKCdelta)(+) interneurons, likely "off cells." Chemogenetic inactivation of Scgn(+)/PKCdelta(+) cells augmented conditioned response to perceived danger in vivo. While Ca(2+)-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. |
