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首页> 外文期刊>Neuron >Membrane lipids tune synaptic transmission by direct modulation of presynaptic potassium channels
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Membrane lipids tune synaptic transmission by direct modulation of presynaptic potassium channels

机译：膜脂质通过直接调节突触前钾通道来调节突触传递

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摘要

Voltage-gated potassium (Kv) channels are involved in action potential (AP) repolarization in excitable cells. Exogenous application of membrane-derived lipids, such as arachidonic acid (AA), regulates the gating of Kv channels. Whether membrane-derived lipids released under physiological conditions have an impact on neuronal coding through this mechanism is unknown. We show that AA released in anactivity-dependent manner from postsynaptic hippocampal CA3 pyramidal cells acts as retrograde messenger, inducing a robust facilitation of mossy fiber (Mf) synaptic transmission over several minutes. AA acts by broadening presynaptic APs through thedirect modulation of Kv channels. This form of short-term plasticity can be triggered when postsynaptic cell fires with physiologically relevant patterns and sets the threshold for the induction of the presynaptic form of long-term potentiation (LTP) at hippocampal Mf synapses. Hence, direct modulation ofpresynaptic Kv channels by activity-dependent release of lipids serves as a physiological mechanism for tuning synaptic transmission.
机译：电压门控钾（Kv）通道参与可激发细胞的动作电位（AP）复极化。膜源性脂质（如花生四烯酸（AA））的外源应用可调节Kv通道的门控。尚不清楚在生理条件下释放的源自膜的脂质是否通过这种机制对神经元编码产生影响。我们表明，AA的活动依赖方式从突触后海马CA3锥体细胞释放作为逆行使者，在几分钟内诱导生苔纤维（Mf）突触传递的强大促进作用。 AA通过直接调制Kv通道来扩大突触前AP的作用。当具有生理学相关模式的突触后细胞着火并触发海马Mf突触诱导突触前形式长期增强（LTP）的阈值时，可以触发这种形式的短期可塑性。因此，通过脂质的活性依赖性释放来直接调节突触前Kv通道作为调节突触传递的生理机制。

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