Sleep is a nearly universal behaviour with unclear functions¹. The synaptic homeostasis hypothesis proposes that sleep is required to renormalize the increases in synaptic number and strength that occur during wakefulness². Some studies examining either large neuronal populations³ or small patches of dendrites⁴ have found evidence consistent with the synaptic homeostasis hypothesis, but whether sleep merely functions as a permissive state or actively promotes synaptic downregulation at the scale of whole neurons is unclear. Here, by repeatedly imaging all excitatory synapses on single neurons across sleep–wake states of zebrafish larvae, we show that synapses are gained during periods of wake (either spontaneous or forced) and lost during sleep in a neuron-subtype-dependent manner. However, synapse loss is greatest during sleep associated with high sleep pressure after prolonged wakefulness, and lowest in the latter half of an undisrupted night. Conversely, sleep induced pharmacologically during periods of low sleep pressure is insufficient to trigger synapse loss unless adenosine levels are boosted while noradrenergic tone is inhibited. We conclude that sleep-dependent synapse loss is regulated by sleep pressure at the level of the single neuron and that not all sleep periods are equally capable of fulfilling the functions of synaptic homeostasis.

睡眠是一种近乎普遍的行为，其功能尚不明确¹。突触稳态假说提出，睡眠需要使清醒期间发生的突触数量和强度的增加重新正常化²。一些研究检查大神经元群^{​​ 3}或小块树突⁴发现了与突触稳态假说一致的证据，但睡眠是否仅仅作为一种允许状态或积极促进整个神经元范围内的突触下调尚不清楚。在这里，通过对斑马鱼幼虫睡眠-觉醒状态下单个神经元上的所有兴奋性突触进行重复成像，我们发现突触在觉醒期间（自发或强迫）获得并在睡眠期间以神经元亚型依赖的方式丢失。然而，突触损失在睡眠期间最大，与长时间清醒后的高睡眠压力相关，并且在不受干扰的夜晚后半段损失最小。相反，在低睡眠压力期间药物诱导的睡眠不足以引发突触损失，除非腺苷水平升高，同时去甲肾上腺素能张力受到抑制。我们得出的结论是，睡眠依赖性突触丢失是由单个神经元水平的睡眠压力调节的，并且并非所有睡眠周期都同样能够实现突触稳态的功能。