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首页> 外文期刊>The European Journal of Neuroscience >Metabotropic glutamate receptors (mGluR5) activate transient receptor potential canonical channels to improve the regularity of the respiratory rhythm generated by the pre-B?tzinger complex in mice
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Metabotropic glutamate receptors (mGluR5) activate transient receptor potential canonical channels to improve the regularity of the respiratory rhythm generated by the pre-B?tzinger complex in mice

机译：代谢型谷氨酸受体（mGluR5）激活瞬时受体电位的规范通道，以改善小鼠前B？tzinger复合物产生的呼吸节律的规律性

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Metabotropic glutamate receptors (mGluRs) are hypothesized to play a key role in generating the central respiratory rhythm and other rhythmic activities driven by central pattern generators (e.g. locomotion). However, the functional role of mGluRs in rhythmic respiratory activity and many motor patterns is very poorly understood. Here, we used mouse respiratory brain-slice preparations containing the pre-B?tzinger complex (pre-B?tC) to identify the role of group I mGluRs (mGluR1 and mGluR5) in respiratory rhythm generation. We found that activation of mGluR1/5 is not required for the pre-B?tC to generate a respiratory rhythm. However, our data suggest that mGluR1 and mGluR5 differentially modulate the respiratory rhythm. Blocking endogenous mGluR5 activity with 2-Methyl-6-(phenylethynyl)pyridine (MPEP) decreases the inspiratory burst duration, burst area and frequency, whereas it increases the irregularity of the fictive eupneic inspiratory rhythm generated by the pre-B?tC. In contrast, blocking mGluR1 reduces the frequency. Moreover, the mGluR1/5 agonist 3,5-dihydroxyphenylglycine increases the frequency and decreases the irregularity of the respiratory rhythm. Based on previous studies, we hypothesized that mGluR signaling decreases the irregularity of the respiratory rhythm by activating transient receptor potential canonical (TRPC) channels, which carry a non-specific cation current (ICAN). Indeed, 3,5-dihydroxyphenylglycine (DHPG) application reduces cycle-by-cycle variability and subsequent application of the TRPC channel blocker 1-[2-(4-methoxyphenyl)-2-[3-(4-methoxyphenyl)propoxy]ethyl]imidazole (SKF-96365) hydrochloride reverses this effect. Our data suggest that mGluR5 activation of ICAN-carrying TRPC channels plays an important role in governing the cycle-by-cycle variability of the respiratory rhythm. These data suggest that modulation of TRPC channels may correct irregular respiratory rhythms in some central neuronal diseases.
机译：假设代谢型谷氨酸受体（mGluRs）在产生中央呼吸节律和由中央模式发生器驱动的其他节律活动（例如运动）中起关键作用。但是，人们对mGluRs在节律性呼吸活动和许多运动模式中的功能作用了解甚少。在这里，我们使用了含有前B？tzinger复合体（pre-B？tC）的小鼠呼吸脑切片制剂，以鉴定I组mGluRs（mGluR1和mGluR5）在呼吸节律产生中的作用。我们发现，激活前B？tC不需要mGluR1 / 5的激活即可产生呼吸节律。但是，我们的数据表明mGluR1和mGluR5差异性调节呼吸节律。用2-甲基-6-（苯基乙炔基）吡啶（MPEP）阻断内源性mGluR5活性可减少吸气爆发持续时间，爆发面积和频率，而增加B-tC之前产生的假性紫杉吸气节律的不规则性。相反，阻断mGluR1降低了频率。此外，mGluR1 / 5激动剂3,5-二羟基苯基甘氨酸增加了频率并降低了呼吸节律的不规则性。基于先前的研究，我们假设mGluR信号传导通过激活携带非特异性阳离子电流（ICAN）的瞬时受体电位经典（TRPC）通道减少呼吸节律的不规则性。确实，3,5-二羟基苯基甘氨酸（DHPG）的应用降低了逐周期变化，并降低了TRPC通道阻滞剂1- [2-（4-甲氧基苯基）-2- [3-（4-甲氧基苯基）丙氧基]乙基的后续应用盐酸]咪唑（SKF-96365）可逆转此作用。我们的数据表明，携带ICAN的TRPC通道的mGluR5激活在控制呼吸节律的逐周期变化中起重要作用。这些数据表明，在某些中枢神经元疾病中，对TRPC通道的调节可能会纠正不规则的呼吸节律。

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