CaMKIIα knockdown decreases anxiety in the open field and low serotonin-induced upregulation of GluA1 in the basolateral amygdala
| Autor: | Lee Tran, N. Bradley Keele |
|---|---|
| Rok vydání: | 2016 |
| Předmět: |
Male
0301 basic medicine Serotonin medicine.medical_specialty 5 7-Dihydroxytryptamine Calcium-Calmodulin-Dependent Protein Kinase Kinase AMPA receptor Anxiety Serotonergic Amygdala Article Open field Rats Sprague-Dawley 03 medical and health sciences Behavioral Neuroscience chemistry.chemical_compound Serotonin Agents 0302 clinical medicine Internal medicine Ca2+/calmodulin-dependent protein kinase medicine Animals Receptors AMPA Phosphorylation 5-HT receptor Basolateral Nuclear Complex Chemistry Rats Up-Regulation 030104 developmental biology Endocrinology medicine.anatomical_structure Neuroscience 030217 neurology & neurosurgery Basolateral amygdala |
| Zdroj: | Behavioural Brain Research. 303:152-159 |
| ISSN: | 0166-4328 |
| DOI: | 10.1016/j.bbr.2016.01.053 |
| Popis: | Hyperactivation of the amygdala is implicated in anxiety and mood disorders, but the precise underlying mechanisms are unclear. We previously reported that depletion of serotonin (5-hydroxytryptamine, 5-HT) in the basolateral nucleus of the amygdala (BLA) using the serotonergic neurotoxin 5,7-dihydroxytryptamine (5,7-DHT) potentiated learned fear and increased glutamate receptor (Glu) expression in BLA. Here we investigated the hypothesis that CaMKII facilitates anxiety-like behavior and increased Glu/AMPA receptor subunit A1 (GluA1) expression following depletion of 5-HT in the BLA. Infusion of 5,7-DHT into the BLA resulted in anxiety-like behavior in the open field test (OFT) and increased the phosphorylation of CaMKIIα (Thr-286) in the BLA. Knockdown of the CaMKIIα subunit using adeno-associated virus (AAV)-delivered shRNAi concomitantly attenuated anxiety-like behavior in the OFT and decreased GluA1 expression in the BLA. Our results suggest that the CaMKII signaling plays a key role in low 5-HT-induced anxiety and mood disturbances, potentially through regulation of GluA1 expression in the BLA. |
| Databáze: | OpenAIRE |
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