Facial stimulation induces long-term depression at cerebellar molecular layer interneuron-Purkinje cell synapses in vivo in mice.
Facial stimulation induces long-term depression at cerebellar molecular layer interneuron-Purkinje cell synapses in vivo in mice.
复制标题
面部刺激会在小鼠体内诱导小脑分子层中间神经元-浦肯野细胞突触的长期抑制。
DOI：
10.3389/fncel.2015.00214
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发表时间：
2015
影响因子：
5.3
通讯作者：
Qiu DL
中科院分区：
文献类型：
--
作者：
Bing YH;Wu MC;Chu CP;Qiu DL
小脑长期突触可塑性为运动学习提供了一种细胞机制。大量研究证实了平行纤维-浦肯野细胞（PF-PC）、平行纤维-分子层中间神经元（PF-MLI）和苔藓纤维-颗粒细胞（MF-GC）突触可塑性的诱导及其机制，但尚未有研究探讨感觉刺激诱发的活体动物小脑皮层平行纤维-分子层中间神经元突触可塑性。采用细胞贴壁法和药理学方法研究了氨基甲酸乙酯麻醉小鼠连续面部刺激诱导MLI-PC gaba能突触可塑性的表达及其机制。我们发现，1 Hz而不是2 Hz或4 Hz的面部刺激会导致中脑-中脑突触gaba能传递的长期抑制（LTD），并伴随着刺激引起的中脑突触spike放电暂停的减少，但不会引起中脑-中脑突触感觉诱发的spike事件的性质发生显著变化。MLI-PC GABAergic LTD可以通过阻断大麻素1型（CB1）受体来预防，并且可以由CB1受体激动剂诱导。此外，在代谢性谷氨酸受体1 （mGluR1）拮抗剂JNJ16259685存在的1hz面部刺激下，仍然诱导了MLI-PC GABAergic LTD，而在1hz面部刺激期间阻断n -甲基- d -天冬氨酸（NMDA）受体可消除MLI-PC GABAergic LTD的表达。这些结果表明，感觉刺激可以通过激活小鼠小脑皮质小腿II区的NMDA受体，诱导内源性大麻素（eCB）依赖性的gaba能在MLI-PC突触传递。我们的研究结果表明，感觉刺激诱发的MLI-PC gaba能突触可塑性可能在动物运动学习中起关键作用。
Cerebellar long-term synaptic plasticity has been proposed to provide a cellular mechanism for motor learning. Numerous studies have demonstrated the induction and mechanisms of synaptic plasticity at parallel fiber–Purkinje cell (PF–PC), parallel fiber–molecular layer interneurons (PF–MLI) and mossy fiber–granule cell (MF–GC) synapses, but no study has investigated sensory stimulation-evoked synaptic plasticity at MLI–PC synapses in the cerebellar cortex of living animals. We studied the expression and mechanism of MLI–PC GABAergic synaptic plasticity induced by a train of facial stimulation in urethane-anesthetized mice by cell-attached recordings and pharmacological methods. We found that 1 Hz, but not a 2 Hz or 4 Hz, facial stimulation induced a long-term depression (LTD) of GABAergic transmission at MLI–PC synapses, which was accompanied with a decrease in the stimulation-evoked pause of spike firing in PCs, but did not induce a significant change in the properties of the sensory-evoked spike events of MLIs. The MLI–PC GABAergic LTD could be prevented by blocking cannabinoid type 1 (CB1) receptors, and could be pharmacologically induced by a CB1 receptor agonist. Additionally, 1 Hz facial stimulation delivered in the presence of a metabotropic glutamate receptor 1 (mGluR1) antagonist, JNJ16259685, still induced the MLI–PC GABAergic LTD, whereas blocking N-methyl-D-aspartate (NMDA) receptors during 1 Hz facial stimulation abolished the expression of MLI–PC GABAergic LTD. These results indicate that sensory stimulation can induce an endocannabinoid (eCB)-dependent LTD of GABAergic transmission at MLI–PC synapses via activation of NMDA receptors in cerebellar cortical Crus II in vivo in mice. Our results suggest that the sensory stimulation-evoked MLI–PC GABAergic synaptic plasticity may play a critical role in motor learning in animals.
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影响因子：
16.2
作者：
Kawaguchi, S;Hirano, T
通讯作者：
Hirano, T
影响因子：
5.3
作者：
Carter, AG;Regehr, WG
通讯作者：
Regehr, WG
体内小鼠小脑皮质 Crus II 浦肯野细胞中触觉刺激引起的突触反应
影响因子：
3.7
作者：
Chu CP;Bing YH;Liu QR;Qiu DL
通讯作者：
Qiu DL
影响因子：
5.3
作者：
Kawaguchi, S;Hirano, T
通讯作者：
Hirano, T
影响因子：
5.3
作者：
Hardingham, Neil;Fox, Kevin
通讯作者：
Fox, Kevin