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首页> 外文期刊>The European Journal of Neuroscience >NAAG inhibits KCl-induced ((3)H)-GABA release via mGluR3, cAMP, PKA and L-type calcium conductance.
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NAAG inhibits KCl-induced ((3)H)-GABA release via mGluR3, cAMP, PKA and L-type calcium conductance.

机译：NAAG通过mGluR3，cAMP，PKA和L型钙电导抑制KCl诱导的（（3）H）-GABA释放。

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摘要

The peptide neurotransmitter, N-acetylaspartylglutamate (NAAG), is a selective agonist at the type 3 metabotropic glutamate receptor (mGluR3) where it acts to decrease cAMP levels. Rat cortical interneurons express both NAAG and glutamic acid decarboxylase, as well as mGluR3 mRNA. In the presence of ionotropic glutamate receptor antagonists, both NAAG and the group II metabotropic glutamate receptor agonist, DCG-IV, reduced the calcium-dependent, KCl-induced [(3)H]-GABA release from rat cortical neurons by 35%. This release process was unaffected by tetrodotoxin. The group II antagonist, ethyl glutamate, reversed the effects of DCG-IV and NAAG. The mGluR3-selective antagonist, beta-N-acetylaspartylglutamate, reversed the effect of NAAG. While pretreatment of cortical neurons with forskolin alone did not significantly affect KCl-stimulated [(3)H]-GABA-release, forskolin abolished the inhibition of release produced by NAAG. The protein kinase A inhibitor, H-89, decreased [(3)H]-GABA release while NAAG produced no additional inhibition in the presence of H-89. In contrast, the protein kinase C inhibitor, Ro 31--8220, had no effect on KCl-stimulated release, nor did it affect the inhibition of release produced by NAAG. The L-type calcium channel blocker, nifedipine, also inhibited the release of [(3)H]-GABA and coapplication with NAAG resulted in no significant additional inhibition of release. These data support the hypothesis that the inhibition of KCl-stimulated [(3)H]-GABA release by NAAG is mediated via presynaptic mGluR3 on GABAergic cortical neurons and that this effect is obtained by decreasing cAMP with a consequent decrease in protein kinase A activity and L-type calcium channel conductance.
机译：肽神经递质N-乙酰天冬氨酰谷氨酸（NAAG）是3型代谢型谷氨酸受体（mGluR3）的选择性激动剂，可降低cAMP水平。大鼠皮质神经元表达NAAG和谷氨酸脱羧酶，以及mGluR3 mRNA。在存在离子型谷氨酸受体拮抗剂的情况下，NAAG和II型代谢型谷氨酸受体激动剂DCG-IV均能降低钙依赖性的KCl诱导的[（3）H] -GABA从大鼠皮质神经元的释放，降低了35％。该释放过程不受河豚毒素的影响。 II组拮抗剂谷氨酸乙酯逆转了DCG-IV和NAAG的作用。 mGluR3选择性拮抗剂β-N-乙酰基天冬氨酰谷氨酸逆转了NAAG的作用。虽然单独用福司可林预处理皮质神经元不会显着影响KCl刺激的[（3）H] -GABA释放，但福司可林取消了NAAG产生的释放抑制作用。蛋白激酶A抑制剂H-89降低[（3）H] -GABA的释放，而NAAG在H-89的存在下不产生其他抑制作用。相反，蛋白激酶C抑制剂Ro 31--8220对KCl刺激的释放没有影响，也不影响NAAG产生的释放抑制。 L型钙通道阻滞剂硝苯地平也抑制[（3）H] -GABA的释放，与NAAG并用不会导致明显的释放抑制。这些数据支持以下假设：NAAG对KCl刺激的[（3）H] -GABA释放的抑制作用是通过突触前mGluR3对GABA能皮质神经元介导的，并且这种作用是通过降低cAMP从而降低蛋白激酶A活性而获得的。和L型钙通道电导。

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