[대학원 생명과학과 세미나 안내]
연사 : 김정훈 교수(포스텍 생명과학과)
연제 : PV inhibitory neurons-mediated feedforward inhibition onto neural ensembles for the precision of fear memory
일시 : 2022년 06월 10일 (금) 오후 4시 30분
장소 : 대면 및 온라인 화상 강의로 진행됩니다.
초청교수 : 백자현 교수
Abstract
Silent synapses harboring N-methyl-D-aspartate receptors (NMDARs) but no α-amino-3-hydroxy-5-methyl-4- isoxazole propionic acid receptors (AMPARs), are mainly observed during the developmental stages. Interestingly, these silent synapses are resurgent when subjected to addictive drugs. Striatal medium spiny neurons (MSNs) have pivotal roles in addiction progress with divergent neuronal inputs, including dopaminergic and glutamatergic transmission. Glutamatergic inputs to the medium spiny neurons (MSNs) of the Nucleus Accumbens, a critical node for behavioral responses to addictive drugs, are drastically altered by repeated exposure to cocaine. The MSNs are comprised of D1R and D2R-expressing cells in a similar ratio, but cocaine could trigger formation of silent synapses primarily at D1R-MSNs, which requires de novo synthesis of GluN2B. Despite a number of correlative evidence, however, it remains still ambiguous whether and how silent synapses are indispensable for arising of addictive behaviors. GluN2B encoded gene, GRIN2B, is lethal and critical for neuronal development. We took advantage of cre inducible shRNA or CRISPR-Cas9 mediated GluN2B depletion that enables cell type (D1R-MSNs) and area-specific (shell area) modulation without unwanted effects, such as developmental or global KO impacts of target gene deletion. We will discuss the role of GluN2B in the cocaine induced silent synapse formation and subsequent differences in behavioral expression by relatively precise modulation of GluN2B expression.