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首页> 外文期刊>The European Journal of Neuroscience >Properties of 4 Hz stimulation-induced parallel fiber-Purkinje cell presynaptic long-term plasticity in mouse cerebellar cortex in vivo
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Properties of 4 Hz stimulation-induced parallel fiber-Purkinje cell presynaptic long-term plasticity in mouse cerebellar cortex in vivo

机译：4 Hz刺激诱导的小鼠小脑皮质平行纤维-Purkinje细胞突触前长期可塑性的特性

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摘要

Cerebellar parallel fiber-Purkinje cell (PF-PC) long-term synaptic plasticity is important for the formation and stability of cerebellar neuronal circuits, and provides substrates for motor learning and memory. We previously reported both presynaptic long-term potentiation (LTP) and long-term depression (LTD) in cerebellar PF-PC synapses in vitro. However, the expression and mechanisms of cerebellar PF-PC synaptic plasticity in the cerebellar cortex in vivo are poorly understood. In the present study, we studied the properties of 4 Hz stimulation-induced PF-PC presynaptic long-term plasticity using in vivo the whole-cell patch-clamp recording technique and pharmacological methods in urethane-anesthetised mice. Our results demonstrated that 4 Hz PF stimulation induced presynaptic LTD of PF-PC synaptic transmission in the intact cerebellar cortex in living mice. The PF-PC presynaptic LTD was attenuated by either the N-methyl-D-aspartate receptor antagonist, D-aminophosphonovaleric acid, or the group 1 metabotropic glutamate receptor antagonist, JNJ16259685, and was abolished by combined D-aminophosphonovaleric acid and JNJ16259685, but enhanced by inhibition of nitric oxide synthase. Blockade of cannabinoid type 1 receptor activity abolished the PF-PC LTD and revealed a presynaptic PF-PC LTP. These data indicate that both endocannabinoids and nitric oxide synthase are involved in the 4 Hz stimulation-induced PF-PC presynaptic plasticity, but the endocannabinoid-dependent PF-PC presynaptic LTD masked the nitric oxide-mediated PF-PC presynaptic LTP in the cerebellar cortex in urethane-anesthetised mice.
机译：小脑平行纤维-浦肯野细胞（PF-PC）的长期突触可塑性对于小脑神经元回路的形成和稳定性很重要，并为运动学习和记忆提供了基础。我们先前曾报道小脑PF-PC突触在体外的突触前长期增强（LTP）和长期抑郁（LTD）。但是，小脑PF-PC突触可塑性在体内的表达和机制尚不清楚。在本研究中，我们使用全细胞膜片钳记录技术和药理学方法在氨基甲酸乙酯麻醉的小鼠体内研究了4 Hz刺激诱导的PF-PC突触前突触长期可塑性。我们的研究结果表明4 Hz PF刺激在活小鼠的完整小脑皮质中诱导了PF-PC突触传递的突触前LTD。 PF-PC突触前LTD被N-甲基-D-天冬氨酸受体拮抗剂D-氨基膦酸戊酸或第1组代谢型谷氨酸受体拮抗剂JNJ16259685减弱，并被D-氨基膦酸戊酸和JNJ16259685联合废除，但通过抑制一氧化氮合酶增强。大麻素1型受体活性的阻断消除了PF-PC LTD，并揭示了突触前的PF-PC LTP。这些数据表明内源性大麻素和一氧化氮合酶均参与4 Hz刺激诱导的PF-PC突触前突触可塑性，但内源性大麻素依赖性PF-PC突触前LTD掩盖了小脑皮质中一氧化氮介导的PF-PC突触前LTP。在氨基甲酸乙酯麻醉的小鼠中。

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