2-B-SS09-2 〇齋藤 惇¹、江崎 博仁¹、村田 陽香²、倪 煕焱¹、中條 湧介¹、平野 優紀¹、向井 悠乃¹、西谷 直也^1,2、出山 諭司^1,2、金田 勝幸^1,2 Atsushi Saito¹, Hirohito Esaki¹, Haruka Murata², Xiyan Ni¹, Yusuke Chujo¹, Yuki Hirano¹, Yuno Mukai¹, Naoya Nishitani^1,2, Satoshi Deyama^1,2, Katsuyuki Kaneda^{1,2 1}金沢大・院薬・薬理、²金沢大・薬・薬理 ¹Lab. Mol. Pharmacol., Inst. Med., Pharmaceut., Health Sci., Kanazawa Univ., ²Lab. Mol. Pharmacol., Sch. Pharmaceut. Sci., Kanazawa Univ. Stress potentiates cocaine craving by enhancing the rewarding effects of cocaine, yet the mechanisms underlying this process remain unclear. To address this issue, we examined the role of dopaminergic transmission in the medial prefrontal cortex (mPFC) and basolateral amygdala (BLA), and of reciprocal interaction between these nuclei, using a cocaine conditioned place preference (CPP) paradigm combined with acute social defeat (SD) stress in mice. Brief SD exposure before the posttest enhanced cocaine CPP, which was significantly suppressed by systemic, bilateral intra-mPFC, or bilateral intra-BLA injection of SCH23390 (SCH), a dopamine D1 receptor antagonist. Unilateral mPFC and contralateral BLA injections of SCH also suppressed the stress-induced CPP enhancement, suggesting the dopaminergic modulation of reciprocal glutamatergic connection between the mPFC and BLA. Accordingly, simultaneous injections of SCH into the unilateral mPFC and NBQX, an AMPA receptor antagonist, into the contralateral BLA, inhibited the enhanced CPP. By contrast, simultaneous infusions of NBQX to the unilateral mPFC and SCH to the contralateral BLA failed to affect the CPP enhancement. Moreover, selective inhibition of glutamatergic projections from the mPFC to the BLA with the chemogenetic technique suppressed the enhancement of CPP. These findings suggest that dopaminergic inputs to the mPFC and BLA may modulate glutamatergic transmission from the mPFC to BLA, but not from the BLA to mPFC, which contributes to stress-induced potentiation of cocaine craving.