Regulation of synaptic plasticity and learning by cross-talk of G protein-coupled receptors

我们对培养的小鼠小脑浦肯野细胞的电生理分析表明，配体激活的腺苷A1受体（A1 R）通过降低1型代谢型谷氨酸受体（mGluR 1）的谷氨酸敏感性来阻止小脑长时程抑郁（LTD），我们的体内行为分析表明，B型γ-氨基丁酸受体（GABAbR）的激活，促进小脑LTD依赖性运动学习。这些研究结果表明，在响应于脑脊髓液中的神经调质，A1 R和GABAbR调节mGluR 1，从而调节突触可塑性和学习的诱导。

Our electrophysiological analyses in cultured mouse cerebellar Purkinje cells suggest that ligand-activated adenosine A1 receptor (A1R) impedes cerebellar long-term depression (LTD) by decreasing the glutamate-sensitivity of type-1 metabotropic glutamate receptor (mGluR1), a key trigger of induction of cerebellar LTD. Our in-vivo behavioral analyses showed that activation of B-type gamma-amino butyric acid receptor (GABAbR) facilitated cerebellar LTD-dependent motor learning. These findings suggest that in response to neuromodulators in the cereberospinal fluid, A1R and GABAbR modulate mGluR1 and thereby regulate induction of synaptic plasticity and learning.