Mitoma H, Konishi S
Mitsubishi Kasei Institute of Life Sciences, Tokyo, Japan.
Neurosci Lett. 1996 Oct 18;217(2-3):141-4.
Roles of monoaminergic neurons in synaptic plasticity are not well clarified at mammalian central synapses. We therefore examined the actions of serotonin and noradrenaline on cerebellar excitatory and inhibitory synapses using the whole-cell recording with rat cerebellar slices. Applications of the two amines selectively elicited long-lasting facilitation of gamma-aminobutyric acid (GABA)-mediated inhibitory transmission, possibly through a presynaptic mechanism. The facilitatory action of the amines on GABAergic transmission was mimicked by forskolin and blocked by protein kinase inhibitors, suggesting the involvement of cyclic AMP (cAMP)-dependent mechanism in their action. A monoamine uptake inhibitor, imipramine, enhanced the GABAergic transmission, whereas it was suppressed by monoamine receptor antagonists, propranolol and methiothepin, suggesting that endogenous monoamines released by stimulation enhance the inhibitory transmission at cerebellar GABAergic synapses in sustained and activity-dependent manner. Such monoaminergic facilitation may provide a likely mechanism for synaptic plasticity in motor coordination within the mammalian cerebellar function.
单胺能神经元在哺乳动物中枢突触的突触可塑性中的作用尚未得到充分阐明。因此，我们使用大鼠小脑切片的全细胞记录技术，研究了血清素和去甲肾上腺素对小脑兴奋性和抑制性突触的作用。这两种胺类物质的应用选择性地引发了γ-氨基丁酸（GABA）介导的抑制性传递的持久增强，可能是通过一种突触前机制。胺类物质对GABA能传递的促进作用可被福斯高林模拟，并被蛋白激酶抑制剂阻断，这表明其作用涉及环磷酸腺苷（cAMP）依赖性机制。一种单胺摄取抑制剂丙咪嗪增强了GABA能传递，而单胺受体拮抗剂普萘洛尔和甲硫哒嗪则抑制了这种增强，这表明刺激释放的内源性单胺以持续且依赖活动的方式增强了小脑GABA能突触的抑制性传递。这种单胺能促进作用可能为哺乳动物小脑功能中运动协调的突触可塑性提供了一种可能的机制。
