学習性無力感形成における分界条床核のNMDA型グルタミン酸受容体の役割

• Published in: 日本薬理学会年会要旨集 p. 3-P-292
• Main Authors: 前田, 桜, 菅野, 美樹, 森谷, 美穂, 橋本, 璃乃, 福和田, 奈緒, 関, 健二郎, 松木, 亨
• Format: Journal Article
• Language: Japanese
• Published: 公益社団法人 日本薬理学会 2020
• Subjects: behavior; depression; lipopolysaccharide; N-methyl-D-aspartate (NMDA) receptor
• ISSN: 2435-4953
• DOI: 10.1254/jpssuppl.93.0_3-P-292

The synaptic plasticity in the bed nucleus of stria terminalis (BNST) is induced by the activation of α1 and β-adrenergic receptors, and/or NMDA receptors. We previously reported the possibility that the synaptic plasticity in BNST contributes to the induction of depressive-like behavior, because the α1 and β-receptors in BNST regulated the learned despairs in mice. However, neither α1 nor β-receptors in BNST affected the lipopolysaccharide (LPS)-induced behavioral despair in mice. Therefore, we investigated whether the NMDA receptors in BNST contribute to the induction of LPS-induced behavioral despair. The bilateral intra-BNST pretreatment of MK-801, a NMDA receptor antagonist, 30 min prior to LPS injection, decreased the immobility time during tail suspension test (TST) 24 hours after the LPS challenging. In consistent, bilateral intra-BNST injection of NMDA (24 mg/125 nl/side) slightly shortened the immobility time during TST. However, bilateral intra-BNST co-injection of muscimol (75 ng/125 nl/side), a GABAA receptor agonist, with NMDA potently decreased the immobility time during TST. Because this dose of muscimol alone did not affect the immobility time of TST, in the present study, we suggest that the activation of NMDA receptors with GABAA receptors in BNST is important for the induction of depressive-like behavior.