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首页> 外文期刊>eLife journal >Characterization of developmental and molecular factors underlying release heterogeneity at Drosophila synapses
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Characterization of developmental and molecular factors underlying release heterogeneity at Drosophila synapses

机译:果蝇突触释放异质性的发育和分子因素的表征

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摘要

To send a message to its neighbor, a neuron releases chemicals called neurotransmitters into the gap – or synapse – between them. The neurotransmitter molecules bind to proteins on the receiver neuron called receptors. But what causes the sender neuron to release neurotransmitter in the first place? The process starts when an electrical impulse called an action potential arrives at the sender cell. Its arrival causes channels in the membrane of the sender neuron to open, so that calcium ions flood into the cell. The calcium ions interact with packages of neurotransmitter molecules, known as synaptic vesicles. This causes some of the vesicles to empty their contents into the synapse. But this process is not particularly reliable. Only a small fraction of action potentials cause vesicles to fuse with the synaptic membrane. How likely this is to occur varies greatly between neurons, and even between synapses formed by the same neuron. Synapses that are likely to release neurotransmitter are said to be strong. They are good at passing messages from the sender neuron to the receiver. Synapses with a low probability of release are said to be weak. But what exactly differs between strong and weak synapses? Akbergenova et al. studied synapses between motor neurons and muscle cells in the fruit fly Drosophila. Each motor neuron forms several hundred synapses. Some of these synapses are 50 times more likely to release neurotransmitter than others. Using calcium imaging and genetics, Akbergenova et al. showed that sender cells at strong synapses have more calcium channels than sender cells at weak synapses. The subtypes and arrangement of receptor proteins also differ between the receiver neurons of strong versus weak synapses. Finally, studies in larvae revealed that newly formed synapses all start out weak and then gradually become stronger. How fast this strengthening occurs depends on how active the neuron at the synapse is. This study has shown, in unprecedented detail, key molecular factors that make some fruit fly synapses more likely to release neurotransmitter than others. Many proteins at synapses of mammals resemble those at fruit fly synapses. This means that similar factors may also explain differences in synaptic strength in the mammalian brain. Changes in the strength of synapses underlie the ability to learn. Furthermore, many neurological and psychiatric disorders result from disruption of synapses. Understanding the molecular basis of synapses will thus provide clues to the origins of certain brain diseases.
机译:为了向邻居发送消息,神经元将称为神经递质的化学物质释放到它们之间的缝隙或突触中。神经递质分子与受体神经元上的蛋白质结合,称为受体。但是,是什么原因导致发送器神经元首先释放神经递质?当称为动作电位的电脉冲到达发送器单元时,该过程开始。它的到达导致发送神经元膜中的通道打开,从而使钙离子泛滥到细胞中。钙离子与称为突触小泡的神经递质分子的包裹相互作用。这导致一些囊泡将其内含物排空到突触中。但是这个过程不是特别可靠。仅一小部分动作电位导致囊泡与突触膜融合。在神经元之间,甚至在同一神经元形成的突触之间,发生这种可能性的可能性差异很大。据说可能释放神经递质的突触很强。它们擅长将消息从发送者神经元传递到接收者。释放可能性低的突触被认为是弱的。但是强突触和弱突触之间到底有什么不同? Akbergenova等。研究果蝇果蝇运动神经元与肌肉细胞之间的突触。每个运动神经元形成数百个突触。这些突触中的一些释放神经递质的可能性是其他突触的50倍。利用钙成像和遗传学,Akbergenova等。研究表明,强突触的发送细胞比弱突触的发送细胞具有更多的钙通道。受体蛋白的亚型和排列在强突触和弱突触的受体神经元之间也不同。最终,对幼虫的研究表明,新形成的突触全部开始较弱,然后逐渐变得更强。这种强化发生的速度取决于突触上神经元的活跃程度。这项研究以前所未有的细节显示了使某些果蝇突触比其他方式更可能释放神经递质的关键分子因素。哺乳动物突触中的许多蛋白质类似于果蝇突触中的蛋白质。这意味着相似的因素也可以解释哺乳动物大脑中突触强度的差异。突触强度的变化是学习能力的基础。此外,许多神经和精神疾病是由突触破坏引起的。因此,了解突触的分子基础将为某些大脑疾病的起源提供线索。

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