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三磷酸腺苷增强大鼠三叉神经尾侧亚核的神经传递。

ATP potentiates neurotransmission in the rat trigeminal subnucleus caudalis.

作者信息

Jennings Ernest A, Christie MacDonald J, Sessle Barry J

机构信息

Department of Anatomy and Cell Biology, University of Melbourne, Parkville, Victoria, Australia.

出版信息

Neuroreport. 2006 Oct 2;17(14):1507-10. doi: 10.1097/01.wnr.0000234740.97076.95.

DOI:10.1097/01.wnr.0000234740.97076.95
PMID:16957598
Abstract

Ionotropic purine receptors (P2X) have been implicated in nociceptive neurotransmission. In this study, we examine the actions of the P2X receptor agonist alpha,beta methylene adenosine 5'-triphosphate on excitatory neurotransmission in neurons in the deep and superficial laminae of the trigeminal spinal subnucleus caudalis (Vc), which receives nociceptive inputs from the craniofacial region. Alpha, beta methylene adenosine 5'-triphosphate caused an increase in spontaneous excitatory neurotransmission (miniature excitatory postsynaptic currents) in neurons in deep but not superficial laminae of Vc; this effect could be inhibited by the P2X receptor antagonist 2,3-O-2,4,6-trinitrophenyl-ATP. Conversely, the TRPV1 agonist capsaicin caused an increase in miniature excitatory postsynaptic currents in neurons in the superficial but not deep laminae. These data suggest that alpha,beta methylene adenosine 5'-triphosphate acts on presynaptic terminals to increase glutamatergic neurotransmission in deep Vc neurons.

摘要

离子型嘌呤受体(P2X)与伤害性神经传递有关。在本研究中,我们研究了P2X受体激动剂α,β-亚甲基腺苷5'-三磷酸对三叉神经脊束核尾侧亚核(Vc)深层和浅层神经元兴奋性神经传递的作用,该亚核接收来自颅面部区域的伤害性输入。α,β-亚甲基腺苷5'-三磷酸使Vc深层而非浅层神经元的自发性兴奋性神经传递(微小兴奋性突触后电流)增加;这种作用可被P2X受体拮抗剂2,3-O-2,4,6-三硝基苯基-ATP抑制。相反,TRPV1激动剂辣椒素使浅层而非深层神经元的微小兴奋性突触后电流增加。这些数据表明,α,β-亚甲基腺苷5'-三磷酸作用于突触前终末,以增加Vc深层神经元的谷氨酸能神经传递。

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