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首页> 外文期刊>Neurochemistry International: The International Journal for the Rapid Publication of Critical Reviews, Preliminary and Original Research Communications in Neurochemistry >Glutamate differently modulates excitatory and inhibitory adenosine receptors in neuronal and glial cells.
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Glutamate differently modulates excitatory and inhibitory adenosine receptors in neuronal and glial cells.

机译：谷氨酸在神经元和神经胶质细胞中不同地调节兴奋性和抑制性腺苷受体。

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摘要

Adenosine is a neuromodulator which acts through adenosine receptors regulating functions such as inhibition of glutamate release. Adenosine A(1) and A(2A) receptor activations most often regulate opposing actions. Primary rat cortical neurons and rat C6 cells, an astrocytic derived cell line, were exposed to 100muM l-glutamate, and cell viability and transduction pathways mediated by both A(1) and A(2A) receptors were analyzed. Glutamate-induced excitotoxic damage was found only in cortical neurons, with C6 cells preserved. In C6 cells, adenosine A(1) and A(2A) receptors were increased and decreased, respectively. Consequently, A(1)-mediated adenylyl cyclase inhibition and A(2A)-mediated adenylyl cyclase stimulation were, respectively, increased and decreased after glutamate exposure. In cortical neurons, glutamate treatment increased both A(1) and A(2A) receptors. Moreover, adenylyl cyclase responsiveness to A(1) or A(2A) receptor agonists was heightened in these cells, in which pharmacological activation of AC induced cell death. Finally, activation of A(1) receptor or blockade of A(2A) receptor during glutamate treatment partially prevented the glutamate-induced cell death detected in cultured cortical neurons. Results show that adenosine receptors are regulated by glutamate, and that this regulation is dependent on the cell type, suggesting that adenosine receptors might be promising targets in the therapy against excitotoxic cell death.
机译：腺苷是一种神经调节剂，它通过腺苷受体调节功能，例如抑制谷氨酸的释放。腺苷A（1）和A（2A）受体激活最常调节相反的作用。将大鼠原代皮层神经元和大鼠C6细胞（星形细胞来源的细胞系）暴露于100μM1-谷氨酸，并分析了由A（1）和A（2A）受体介导的细胞活力和转导途径。仅在皮质神经元中发现了谷氨酸诱导的兴奋性毒性损伤，并保留了C6细胞。在C6细胞中，腺苷A（1）和A（2A）受体分别增加和减少。因此，谷氨酸暴露后，A（1）介导的腺苷酸环化酶抑制和A（2A）介导的腺苷酸环化酶刺激分别增加和减少。在皮层神经元中，谷氨酸处理增加了A（1）和A（2A）受体。此外，在这些细胞中，腺苷酸环化酶对A（1）或A（2A）受体激动剂的反应性增强，其中AC的药理活化引起细胞死亡。最后，在谷氨酸处理过程中激活A（1）受体或阻断A（2A）受体可部分阻止在培养的皮层神经元中检测到的谷氨酸诱导的细胞死亡。结果表明，腺苷受体受谷氨酸调节，并且该调节依赖于细胞类型，表明腺苷受体可能是抗激毒性细胞死亡的有希望的靶标。

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