Sleep-dependent plasticity requires cortical activity
Sleep-dependent plasticity requires cortical activity
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DOI：
10.1523/jneurosci.2722-05.2005
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发表时间：
2005-10-05
影响因子：
5.3
通讯作者：
Frank, MG
中科院分区：
文献类型：
--
作者：
Jha, SK;Jones, BE;Frank, MG
最近在人类和动物身上的发现表明，睡眠促进突触可塑性，但其潜在机制尚未确定。最近，我们已经证明了睡眠在眼优势（OD）可塑性，一个经典的形式在体内皮质重塑触发单眼剥夺（MD）在发展的关键时期的重要作用。睡眠对OD可塑性影响的机制尚不清楚，但可能取决于睡眠中大脑的神经元活动。我们研究了皮层活动在睡眠依赖性可塑性的作用，可逆性失活睡眠视觉皮层（V1）后一段时间的MD。关键期猫双侧V1和标准EEG/EMG电极中植入套管进行多导睡眠图记录。在一段时间的MD后，视皮层被注入钠通道阻滞剂利多卡因的载体或载体仅在睡眠期间。第三组猫作为假手术对照，在V1外输注利多卡因（进入CSF）。光学成像的内在皮层信号和微电极记录表明，OD可塑性显着降低猫的视觉皮层在睡眠过程中可逆性沉默。这些发现表明，这种形式的睡眠依赖性可塑性的机制需要皮层活动。他们提供了一个重要的洞察睡眠如何修改突触电路缩小范围的可能的候选机制，那些活动依赖。
Recent findings in humans and animals suggest that sleep promotes synaptic plasticity, but the underlying mechanisms have not been identified. We have demonstrated recently an important role for sleep in ocular dominance (OD) plasticity, a classic form of in vivo cortical remodeling triggered by monocular deprivation (MD) during a critical period of development. The mechanisms responsible for the effects of sleep on OD plasticity are unknown but may depend on neuronal activity in the sleeping brain. We investigated the role of cortical activity in sleep-dependent plasticity by reversibly inactivating the sleeping visual cortex (V1) after a period of MD. Critical period cats were bilaterally implanted with cannulas in V1 and standard EEG/EMG electrodes for polysomnographic recording. After a period of MD, visual cortices were infused with the sodium channel blocker lidocaine in vehicle or vehicle only during sleep. A third group of cats served as sham controls and were infused with lidocaine outside of V1 (into the CSF). Both optical imaging of intrinsic cortical signals and microelectrode recordings showed that OD plasticity was significantly reduced in cats whose visual cortices were reversibly silenced during sleep. These findings demonstrate that the mechanisms governing this form of sleep-dependent plasticity require cortical activity. They provide an important insight into how sleep modifies synaptic circuitry by narrowing the range of possible candidate mechanisms to those that are activity dependent.