Sensory information is transferred to the cerebellar cortex via the mossy fiber–granule cell (MF–GC) pathway, which participates in motor coordination and motor learning. We previously reported that chronic ethanol exposure from adolescence facilitated sensory-evoked molecular layer interneuron–Purkinje cell synaptic transmission in adult mice in vivo. Herein, we investigated the effect of chronic ethanol exposure from adolescence on facial stimulation-evoked MF–GC synaptic transmission in the adult mouse cerebellar cortex using electrophysiology recording techniques and pharmacological methods. Chronic ethanol exposure from adolescence induced enhancement of facial stimulation-evoked MF–GC synaptic transmission in the cerebellar cortex of adult mice. Compared with that in control mice, the application of an N-methyl-D-aspartate receptor (NMDAR) antagonist, D-APV (250 μM), induced stronger depression of facial stimulation-evoked MF–GC synaptic transmission in chronic ethanol-exposed mice. Chronic ethanol exposure-induced facilitation of facial stimulation evoked by MF–GC synaptic transmission was abolished by a selective GluN2A antagonist, PEAQX (10 µM) but was unaffected by the application of a selective GluN2B antagonist, TCN-237 (10 µM), or a type 1 metabotropic glutamate receptor blocker, JNJ16259685 (10 μM). These results indicate that chronic ethanol exposure from adolescence enhances facial stimulation-evoked MF–GC synaptic transmission via GluN2A, which suggests that chronic ethanol exposure from adolescence impairs the high-fidelity transmission capability of sensory information in the cerebellar cortex by enhancing the NMDAR-mediated components of MF–GC synaptic transmission in adult mice in vivo

中文翻译：

---

慢性乙醇暴露通过小鼠小脑皮层中的 GluN2A 受体增强面部刺激诱发的苔藓纤维颗粒细胞突触传递

感觉信息通过苔藓纤维颗粒细胞（MF-GC）通路传递到小脑皮层，参与运动协调和运动学习。我们之前曾报道，青春期的慢性乙醇暴露促进了体内成年小鼠的感觉诱发分子层中间神经元-浦肯野细胞突触传递。在此，我们使用电生理记录技术和药理学方法研究了青春期慢性乙醇暴露对成年小鼠小脑皮层中面部刺激诱发的 MF-GC 突触传递的影响。青春期慢性乙醇暴露诱导成年小鼠小脑皮层面部刺激诱发的 MF-GC 突触传递增强。与对照组小鼠相比，N-甲基-D-天冬氨酸受体 (NMDAR) 拮抗剂 D-APV (250 μM) 的应用在慢性乙醇暴露的小鼠中诱导了面部刺激诱发的 MF-GC 突触传递的更强抑制。MF-GC 突触传递引起的面部刺激的慢性乙醇暴露诱导的促进被选择性 GluN2A 拮抗剂 PEAQX (10 µM) 消除，但不受选择性 GluN2B 拮抗剂 TCN-237 (10 µM) 的影响，或1 型代谢型谷氨酸受体阻滞剂，JNJ16259685 (10 μM)。这些结果表明，来自青春期的慢性乙醇暴露通过 GluN2A 增强了面部刺激诱发的 MF-GC 突触传递，