Neuropeptide S inhibits release of 5-HT and glycine in mouse amygdala and frontal/prefrontal cortex through activation of the neuropeptide S receptor

被引:8
作者
Gardella, Elena [1 ]
Romei, Cristina [1 ]
Cavallero, Anna [2 ]
Trapella, Claudio [3 ]
Fedele, Ernesto [1 ,4 ]
Raiteri, Luca [1 ,4 ,5 ]
机构
[1] Univ Genoa, Dept Pharm, Pharmacol & Toxicol Unit, Genoa, Italy
[2] CNR, Inst Biophys, Genoa, Italy
[3] Univ Ferrara, Dept Chem & Pharmaceut Sci, I-44100 Ferrara, Italy
[4] Univ Genoa, Ctr Excellence Biomed Res, Genoa, Italy
[5] Natl Inst Neurosci, Genoa, Italy
关键词
Neuropeptide S; 5-HT release; Glycine release; Amygdala; Frontal/prefrontal cortex; Anxiety; NERVE-ENDINGS; FOOD-INTAKE; RAT-BRAIN; IN-VIVO; SHA; 68; ANXIETY; ANTAGONIST; SYNAPTOSOMES; SEROTONIN; MECHANISMS;
D O I
10.1016/j.neuint.2013.02.003
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Neuropeptide S (NPS) is a neurotransmitter/neuromodulator that has been identified as the natural ligand of G protein-coupled receptors termed NPS receptors (NPSRs). The NPS-NPSR system is involved in the control of numerous centrally-mediated behaviours, including anxiety. As several classical transmitters play a role in fear/anxiety, we here investigated the regulation by NPS of the exocytotic release of 5-hydroxytryptamine (5-HT) and glycine in nerve terminals isolated from mouse frontal/prefrontal cortex and amygdala. Synaptosomes, prelabelled with the tritiated neurotransmitters, were depolarized in superfusion with 12-15 mM KCl and exposed to varying concentrations of NPS. The evoked release of [H-3]5-HT in frontal/prefrontal cortex was potently inhibited by NPS (maximal effect about 25% at 0.1 nM). Differently, the neuropeptide exhibited higher efficacy but much lower potency in amygdala (maximal effect about 40% at 1 mu M). NPS was an extremely potent inhibitor of the K+-evoked release of [H-3]glycine in frontal/prefrontal nerve endings (maximal effect about 25% at 1 pM). All the inhibitory effects observed were counteracted by the NPSR antagonist SHA 68, indicating that the neuropeptide acted at NPSRs. In conclusion, NPS can inhibit the exocytosis of 5-HT and of glycine through the activation of presynaptic NPSRs situated on serotonergic and glycinergic terminals in areas involved in fear/anxiety behaviours. The possibility exists that the NPSRs in frontal/prefrontal cortex are high-affinity receptors involved in non-synaptic transmission, whereas the NPSRs on amygdala serotonergic terminals are low-affinity receptors involved in axo-axonic synaptic communication. (C) 2013 Elsevier Ltd. All rights reserved.
引用
收藏
页码:360 / 366
页数:7
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