Cowen Mara H, Raizen David M, Hart Michael P
Department of Genetics, University of Pennsylvania, Perelman School of Medicine, Philadelphia, PA 19104, USA.
Neuroscience Graduate Group, University of Pennsylvania, Philadelphia, PA 19104, USA.
iScience. 2024 Mar 11;27(4):109477. doi: 10.1016/j.isci.2024.109477. eCollection 2024 Apr 19.
Structural neuroplasticity (changes in the size, strength, number, and targets of synaptic connections) can be modified by sleep and sleep disruption. However, the causal relationships between genetic perturbations, sleep loss, neuroplasticity, and behavior remain unclear. The GABAergic DVB neuron undergoes structural plasticity in adult males in response to adolescent stress, which rewires synaptic connections, alters behavior, and is dependent on conserved autism-associated genes / and We find that four methods of sleep deprivation transiently induce DVB neurite extension in day 1 adults and increase the time to spicule protraction, which is the functional and behavioral output of the DVB neuron. Loss of and prevent DVB structural plasticity and behavioral changes at day 1 caused by adolescent sleep loss. Therefore, and mediate the morphologic and behavioral consequences of sleep loss, providing insight into the relationship between sleep, neuroplasticity, behavior, and neurologic disease.
结构神经可塑性(突触连接的大小、强度、数量和靶点的变化)可被睡眠及睡眠中断所改变。然而,基因扰动、睡眠缺失、神经可塑性和行为之间的因果关系仍不清楚。GABA能的DVB神经元在成年雄性个体中会因青春期应激而发生结构可塑性变化,这会重新连接突触连接、改变行为,且依赖于保守的自闭症相关基因。并且我们发现,四种睡眠剥夺方法会在成年第1天的个体中短暂诱导DVB神经突延伸,并增加棘突伸出的时间,而棘突伸出是DVB神经元的功能和行为输出。[基因名称]缺失会阻止青春期睡眠缺失在成年第1天所导致的DVB结构可塑性和行为变化。因此,[基因名称]介导了睡眠缺失的形态学和行为后果,为深入了解睡眠、神经可塑性、行为和神经疾病之间的关系提供了线索。