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首页> 外文期刊>The European Journal of Neuroscience >Activation of group I metabotropic glutamate receptors enhances efficacy of glutamatergic inputs to neonatal rat hypoglossal motoneurons in vitro.
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Activation of group I metabotropic glutamate receptors enhances efficacy of glutamatergic inputs to neonatal rat hypoglossal motoneurons in vitro.

机译:第一组代谢型谷氨酸受体的激活增强了对新生大鼠舌下运动神经元的谷氨酸能输入的功效。

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Abstract Group I metabotropic glutamate receptors (mGluRs) are the main class of metabotropic receptors expressed in the hypoglossus nucleus. Their role in glutamatergic transmission was investigated using patch-clamp recording from motoneurons in a neonatal rat brainstem slice preparation. After pharmacological block of gamma-aminobutyric acid and glycine-mediated inhibition, under voltage-clamp, the selective group I agonist (RS)-3,5-dihydroxyphenylglycine (DHPG) induced a motoneuron inward current by depressing a leak conductance, and strongly facilitated spontaneous glutamatergic synaptic currents. This effect was blocked by 7-(hydroxyimino)cyclopropa[b]chromen-1a-carboxylate ethyl ester (CPCCOEt) and unaffected by 2-methyl-6-(phenylethynyl)pyridine hydrochloride (MPEP), indicating a role for subtype 1 mGluRs. The frequency but not the amplitude of miniature glutamatergic currents was also enhanced by DHPG. Currents elicited by puffer application of (RS)-alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) in the presence of tetrodotoxin were also unchanged, suggesting that DHPG facilitated release of glutamate. Glutamatergic currents evoked by electrically stimulating the dorsomedullary reticular column premotoneurons were, however, depressed by DHPG in a CPCCOEt-sensitive fashion. Neither CPCCOEt nor MPEP per se changed glutamatergic transmission. Under current-clamp, even if DHPG depressed excitatory postsynaptic potentials, motoneuron spike threshold and time to peak were reduced so that facilitation of synaptic potential/spike coupling became apparent. We propose a wiring diagram to account for the differential action by DHPG on spontaneous and evoked transmission, based on the discrete distribution of subtype 1 mGluRs on glutamatergic afferents. Although under standard recording conditions there was insufficient ambient glutamate to activate mGluRs, such receptors were a powerful target to upregulate excitatory synaptic transmission and enhance signalling by hypoglossal motoneurons to tongue muscles.
机译:摘要I类代谢型谷氨酸受体(mGluRs)是垂体下核中主要表达的代谢型受体。在新生大鼠脑干切片制备中,使用运动神经元的膜片钳记录研究了它们在谷氨酸能传递中的作用。在γ-氨基丁酸的药理学阻断和甘氨酸介导的抑制作用后,在电压钳制下,选择性I组激动剂(RS)-3,5-二羟基苯基甘氨酸(DHPG)通过抑制泄漏电导来诱导运动神经元内向电流,并强烈促进自发的谷氨酸能突触电流。该作用被7-(羟基亚氨基)环丙基[b]铬-1a-羧酸乙酯(CPCCOEt)阻断,不受2-甲基-6-(苯基乙炔基)吡啶盐酸盐(MPEP)的影响,表明其对1型mGluRs具有作用。 DHPG还提高了微型谷氨酸能电流的频率,但没有增加幅度。在河豚毒素的存在下,通过河豚施用(RS)-α-氨基-3-羟基-5-甲基-4-异恶唑丙酸(AMPA)引起的电流也未改变,这表明DHPG促进了谷氨酸的释放。 DHPG以CPCCOEt敏感的方式抑制了通过电刺激背囊性网状柱前神经元而引起的谷氨酸能电流。 CPCCOEt和MPEP本身均未改变谷氨酸能传递。在电流钳下,即使DHPG抑制了兴奋性突触后电位,运动神经元的尖峰阈值和达到峰值的时间也减少了,因此突触电位/突触耦合的促进变得明显。我们提出了一种接线图,以说明DHPG在谷氨酸能受体上亚型1 mGluRs的离散分布的基础上,对自发性和诱发性传递的差异作用。尽管在标准记录条件下,周围谷氨酸不足以激活mGluR,但这类受体是上调兴奋性突触传递并增强舌下运动神经元向舌肌传递信号的强大靶点。

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