Identification of Genes that Maintain Behavioral and Structural Plasticity during Sleep Loss

• Published in: Frontiers in neural circuits Vol. 11; p. 79
• Main Authors: Seugnet, Laurent, Dissel, Stephane, Thimgan, Matthew, Cao, Lijuan, Shaw, Paul J.
• Format: Journal Article
• Language: English
• Published: Switzerland Frontiers Research Foundation 23.10.2017; Frontiers; Frontiers Media S.A
• Subjects: Adults; Animals; Animals, Genetically Modified; Behavioral plasticity; Cognitive ability; Dieldrin; Disease Models, Animal; Drosophila; Drosophila Proteins - genetics; Drosophila Proteins - metabolism; Endopeptidases - genetics; Endopeptidases - metabolism; Homeostasis; Homeostasis - genetics; Homeostasis - physiology; Insects; Insomnia; Learning; Life Sciences; Memory; Memory, Short-Term - physiology; Motor Activity - genetics; Motor Activity - physiology; Mushroom bodies; Mushroom Bodies - metabolism; Mushroom Bodies - pathology; Nerve Tissue Proteins - genetics; Nerve Tissue Proteins - metabolism; Neuronal Plasticity - genetics; Neuronal Plasticity - physiology; Neurons; Neurons - metabolism; Neurons - pathology; Neuroscience; plasticity; Receptors, GABA-A - genetics; Receptors, GABA-A - metabolism; Short term memory; sleep; Sleep deprivation; Sleep Deprivation - genetics; Sleep Deprivation - metabolism; Sleep Deprivation - pathology; Sleep disorders; Sleep Initiation and Maintenance Disorders - genetics; Sleep Initiation and Maintenance Disorders - metabolism; Sleep Initiation and Maintenance Disorders - pathology; Synapses - genetics; Synapses - metabolism; Synapses - pathology; Synaptogenesis; γ-Aminobutyric acid; United States > US; sleep; homeostasis; memory; Drosophila; plasticity; learning; GABA-A receptors; ubiquitin
• ISSN: 1662-5110; 1662-5110
• DOI: 10.3389/fncir.2017.00079

Although patients with primary insomnia experience sleep disruption, they are able to maintain normal performance on a variety of cognitive tasks. This observation suggests that insomnia may be a condition where predisposing factors simultaneously increase the risk for insomnia and also mitigate against the deleterious consequences of waking. To gain insight into processes that might regulate sleep and buffer neuronal circuits during sleep loss, we manipulated three genes, ( , ( ) and the GABA receptor ( ), that were differentially modulated in a model of insomnia. Our results indicate that increasing and decreasing or within wake-promoting large ventral lateral clock neurons (lLNvs) induces sleep loss. As expected, sleep loss induced by decreasing in the lLNvs results in deficits in short-term memory and increases of synaptic growth. However, sleep loss induced by knocking down in the lLNvs protects flies from sleep-loss induced deficits in short-term memory and increases in synaptic markers. Surprisingly, decreasing and within the Mushroom Bodies (MBs) protects against the negative effects of sleep deprivation (SD) as indicated by the absence of a subsequent homeostatic response, or deficits in short-term memory. Together these results indicate that specific genes are able to disrupt sleep and protect against the negative consequences of waking in a circuit dependent manner.