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首页> 外文期刊>The European Journal of Neuroscience >Dopamine and adenosine mediate substance P-induced depression of evoked IPSCs in the rat nucleus accumbens in vitro.
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Dopamine and adenosine mediate substance P-induced depression of evoked IPSCs in the rat nucleus accumbens in vitro.

机译：在体外，多巴胺和腺苷介导物质P诱导的伏隔大鼠核中诱发的IPSC抑制。

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摘要

The major projection cells of the nucleus accumbens (NAc) are under a strong inhibitory influence from GABAergic afferents and depend on afferent excitation to produce their output. We have earlier reported that substance P (SP), a peptide which is colocalized with GABA in these neurons, depresses excitatory synaptic transmission in this nucleus (Kombian, S.B., Ananthalakshmi, K.V.V., Parvathy, S.S. & Matowe, W.C. (2003) J. Neurophysiol., 89, 728-738). In order to better understand the role of this peptide in the synaptic physiology of the NAc, it is important to determine its effects on inhibitory synaptic responses. Using whole-cell recording in rat forebrain slices, we show here that SP also depresses evoked inhibitory postsynaptic currents (IPSCs) in the NAc via intermediate neuromodulators. SP caused a partially reversible, dose-dependent decrease in evoked IPSC amplitude. This effect was present without measurable changes in the holding current, input resistance of recorded cells or decay rate (tau) of IPSCs. It was mimicked by a neurokinin-1 (NK1) receptor-selective agonist, [Sar9, Met (O2)11]-SP, and blocked by an NK1 receptor-selective antagonist, L 732 138. The SP-induced IPSC depression was prevented by SCH23390, a dopamine D1-like receptor antagonist and by 8-cyclopentyltheophylline, an adenosine A1 receptor blocker. Furthermore, the SP effect was also markedly attenuated by exogenous adenosine, dipyridamole, rolipram and barium. These data show that SP, acting on NK1 receptors, depresses inhibitory synaptic transmission indirectly by enhancing extracellular dopamine and adenosine levels. SP therefore acts in the NAc to modulate both excitatory and inhibitory afferent inputs using the same mechanism(s).
机译：伏伏核（NAc）的主要投射细胞受到GABA能传入分子的强烈抑制作用，并依赖传入激发来产生其输出。我们之前已经报道过P物质（SP）是一种与GABA在这些神经元中共定位的肽，可抑制该核中的兴奋性突触传递（Kombian，SB，Ananthalakshmi，KVV，Parvathy，SS和Matowe，WC（2003）J.神经生理学。，89，728-738）。为了更好地了解该肽在NAc突触生理中的作用，重要的是确定其对抑制性突触反应的影响。使用大鼠前脑切片中的全细胞记录，我们在这里显示SP还可以通过中间神经调节剂抑制NAc中诱发的抑制性突触后电流（IPSC）。 SP引起诱发的IPSC幅度的部分可逆的，剂量依赖性的降低。在没有保持电流，记录的单元的输入电阻或IPSC的衰减率（tau）发生可测量变化的情况下，存在该效应。它由神经激肽1（NK1）受体选择性激动剂[Sar9，Met（O2）11] -SP模仿，并由NK1受体选择性拮抗剂L 732 138阻断。预防了SP诱导的IPSC抑制通过多巴胺D1样受体拮抗剂SCH23390和腺苷A1受体阻滞剂8-环戊基茶碱。此外，外源性腺苷，双嘧达莫，咯利普兰和钡也显着减弱了SP作用。这些数据表明，作用于NK1受体的SP通过增强细胞外多巴胺和腺苷水平间接地抑制抑制性突触传递。因此，SP在NAc中发挥作用，使用相同的机制来调节兴奋性和抑制性传入输入。

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