CaMKIIα knockdown decreases anxiety in the open field and low serotonin-induced upregulation of GluA1 in the basolateral amygdala
作者： Lee Tran , N. Bradley Keele
DOI: 10.1016/J.BBR.2016.01.053
关键词:
摘要: Hyperactivation of the amygdala is implicated in anxiety and mood disorders, but precise underlying mechanisms are unclear. We previously reported that depletion serotonin (5-hydroxytryptamine, 5-HT) basolateral nucleus (BLA) using serotonergic neurotoxin 5,7-dihydroxytryptamine (5,7-DHT) potentiated learned fear increased glutamate receptor (Glu) expression BLA. Here we investigated hypothesis CaMKII facilitates anxiety-like behavior Glu/AMPA subunit A1 (GluA1) following 5-HT Infusion 5,7-DHT into BLA resulted open field test (OFT) phosphorylation CaMKIIα (Thr-286) Knockdown adeno-associated virus (AAV)-delivered shRNAi concomitantly attenuated OFT decreased GluA1 Our results suggest signaling plays a key role low 5-HT-induced disturbances, potentially through regulation
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