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首页> 外文期刊>Neuron >Noradrenergic control of associative synaptic plasticity by selective modulation of instructive signals.
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Noradrenergic control of associative synaptic plasticity by selective modulation of instructive signals.

机译：通过选择性调节指示性信号来控制联想突触可塑性的去甲肾上腺素能。

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摘要

Synapses throughout the brain are modified through associative mechanisms in which one input provides an instructive signal for changes in the strength of a second coactivated input. In cerebellar Purkinje cells, climbing fiber synapses provide an instructive signal for plasticity at parallel fiber synapses. Here, we show that noradrenaline activates alpha2-adrenergic receptors to control short-term and long-term associative plasticity of parallel fiber synapses. This regulation of plasticity does not reflect a conventional direct modulation of the postsynaptic Purkinje cell or presynaptic parallel fibers. Instead, noradrenaline reduces associative plasticity by selectively decreasing the probability of release at the climbing fiber synapse, which in turn decreases climbing fiber-evoked dendritic calcium signals. These findings raise the possibility that targeted presynaptic modulation of instructive synapses could provide a general mechanism for dynamic context-dependent modulation of associative plasticity.
机译：整个大脑的突触通过关联机制进行修改，其中一个输入为第二个共同激活输入的强度变化提供指导性信号。在小脑浦肯野细胞中，攀爬纤维突触可为平行纤维突触的可塑性提供指导性信号。在这里，我们显示去甲肾上腺素激活α2-肾上腺素能受体以控制平行纤维突触的短期和长期缔合可塑性。这种可塑性的调节不能反映出突触后浦肯野细胞或突触前平行纤维的常规直接调节。取而代之的是，去甲肾上腺素通过有选择地降低在攀爬纤维突触处释放的可能性而降低了缔合可塑性，这反过来又降低了攀爬纤维诱发的树突状钙信号。这些发现增加了针对性突触的突触前突触调节可为关联可塑性的动态情境依赖性调节提供一般机制的可能性。

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