抑うつ症状発症に及ぼす分界条床核のβ受容体を介したシナプス可塑性の役割

• Published in: 日本薬理学会年会要旨集 p. 3-P-027
• Main Authors: 菅野, 美樹, 福和田, 奈緒, 関, 健二郎
• Format: Journal Article
• Language: Japanese
• Published: 公益社団法人 日本薬理学会 2019
• ISSN: 2435-4953
• DOI: 10.1254/jpssuppl.92.0_3-P-027

We previously reported that the β-adrenoceptor in the bed nucleus of stria terminalis (BNST) regulate the induction of learned despair in mice. It has been reported that the stimulation of β-adrenoceptor with NMDA receptor in BNST causes the long-term synaptic potentiation (LTP). Therefore we investigated whether the β-adrenoceptor dependent LTP in BNST contribute to the lipopolysaccharide (LPS)-induced behavioral despair. We performed bilateral intra-BNST injection of propranolol, a β-adrenoceptor blocker in awake mice 30 min prior to LPS. Bilateral intra-BNST injection of propranolol alone affected neither the immobility time during tail suspension test (TST) nor sucrose preference. However, bilateral intra-BNST injection of propranolol with MK-801, a non-competitive NMDA receptor antagonist, completely prevented the LPS-induced increase in the immobility time during TST. The LPS-decreased body weight, locomotor activity and sucrose preference were not affected by co-applications of propranolol and MK-801. These results indicated the possibility that the β-adrenoceptor and NMDA receptor-dependent LTP in BNST contribute to the LPS-induced behavioral despair.