Involvement of Neurotransmitters in the Action of the Nociceptin/Orphanin FQ Peptide-Receptor System on Passive Avoidance Learning in Rats

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• 作者：Miklós Palotai (1)
  ágnes Adamik (1)
  Gyula Telegdy (1) (2)
  
• 关键词：Nociception/orphanin FQ ; Orphan GPCR SP9155 P550 ; Passive avoidance learning ; Neurotransmitters ; Receptor antagonits
• 刊名：Neurochemical Research
• 出版年：2014
• 出版时间：August 2014
• 年：2014
• 卷：39
• 期：8
• 页码：1477-1483
• 全文大小：671 KB
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• 作者单位：Miklós Palotai (1)
  ágnes Adamik (1)
  Gyula Telegdy (1) (2)
  
  1. Department of Pathophysiology, Faculty of Medicine, University of Szeged, Semmelweis Str. 1, Szeged, 6701, Hungary
  2. MTA-SZTE Neuroscience Research Group of the Hungarian Academy of Sciences, Szeged, Hungary
  
• ISSN：1573-6903

文摘

The nociceptin/orphanin FQ peptide (NOP) receptor and its endogenous ligand plays role in several physiologic functions of the central nervous system, including pain, locomotion, anxiety and depression, reward and drug addiction, learning and memory. Previous studies demonstrated that the NOP-receptor system induces impairment in memory and learning. However, we have little evidence about the underlying neuromodulation. The aim of the present study was to investigate the involvement of distinct neurotransmitters in the action of the selective NOP receptor agonist orphan G protein-coupled receptor (GPCR) SP9155 P550 on memory consolidation in a passive avoidance learning test in rats. Accordingly, rats were pretreated with a nonselective muscarinic acetylcholine receptor antagonist, atropine, a γ-aminobutyric acid subunit A (GABA-A) receptor antagonist, bicuculline, a D2, D3, D4 dopamine receptor antagonist, haloperidol, a nonselective opioid receptor antagonist, naloxone, a non-specific nitric oxide synthase inhibitor, nitro-l-arginine, a nonselective α-adrenergic receptor antagonist, phenoxybenzamine and a β-adrenergic receptor antagonist, propranolol. Atropine, bicuculline, naloxone and phenoxybenzamine reversed the orphan GPCR SP9155 P550-induced memory impairment, whereas propranolol, haloperidol and nitro-l-arginine were ineffective. Our results suggest that the NOP system-induced impairment of memory consolidation is mediated through muscarinic cholinergic, GABA-A-ergic, opioid and α-adrenergic receptors, whereas β-adrenergic, D2, D3, D4-dopaminergic and nitrergic mechanisms are not be implicated.