We investigated the mechanism underlying the anxiolytic actions of the neuropeptide nociceptin/orphanin FQ (N/OFQ) using the elevated plus-maze test and T-maze test. Microinfusions of N/OFQ (10 or 32pmol) into the central amygdala (ACE) increased the time spent in the open arms of the elevated plus-maze (anxiolytic-like effects), whereas microinfusions of N/OFQ (10, 32 or 100 pmol) into the basolateral amygdala (ABL) did not affect the time spent in the open arms. Moreover, microinfusions of N/OFQ (32 pmol) into the ACE impaired escape performance from the open arms of the elevated T-maze (anxiolytic-like effects), but did not change inhibitory avoidance of the open arms. A non-peptidyl N/OFQ receptor (NOP) antagonist, J-113397(1-[(3R,4R)-1-cyclooctylmethyl-3-hydroxymethyl-4-piperidyl]-3-ethyl-1,3-dihydro-2H-benzimidazol-2-one) (10 mg/kg, s.c.), blocked the anxiolytic-like effects induced by N/OFQ. These results indicate that the anxiolytic-like effects of N/OFQ might be due to impaired escape performance from the open arms and it implicates the N/OFQ system within the ACE in the mediation of panic action.

译文

我们使用高架迷宫测试和T迷宫测试研究了神经肽伤害肽/孤儿院蛋白FQ (N/OFQ) 的抗焦虑作用的潜在机制。将N/OFQ (10或32pmol) 微量输注到中央杏仁核 (ACE) 中会增加在高架迷宫的张开臂中花费的时间 (类抗焦虑作用),而N/OFQ的微量输注 (10,32或100 pmol) 进入基底外侧杏仁核 (ABL) 不影响在张开臂上花费的时间。此外,将N/OFQ (32 pmol) 微量注入ACE会损害T迷宫升高的张开臂的逃逸性能 (抗焦虑样作用),但不会改变张开臂的抑制性避免。非肽基N/OFQ受体 (NOP) 拮抗剂,J-113397(1-[(3R,4R)-1-cyclooctylmethyl-3-hydroxymethyl-4-piperidyl]-3-乙基-1,3-二氢-2h-苯并咪唑-2-酮) (10 mg/kg,s.C.),阻断了N/OFQ诱导的抗焦虑作用。这些结果表明,N/OFQ的抗焦虑作用可能是由于张开臂的逃逸性能受损所致,并且它暗示ACE中的N/OFQ系统参与了恐慌行动的调解。

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