Abstract
Sleep disorder is becoming a widespread problem in current society, and is associated with impaired cognition and emotional disorders. Progranulin (PGRN), also known as granulin epithelin precursor, promotes neurite outgrowth and cell survival, and is encoded by the GRN gene. It is a tumor necrosis factor α receptor (TNFR) ligand which is implicated in many central nervous system diseases. However, the role PGRN in sleep disorder remains unclear. In the present study, we found that sleep deprivation (S-DEP) impaired the memory and produced thigmotaxis/anxiety-like behaviors in mice. S-DEP increased the levels of TNFα but decreased PGRN levels in the hippocampus. The intracerebroventricular (ICV) injection of PGRN or intraperitoneal injection of TNFα synthesis blocker thalidomide (25 mg/kg), prevented the memory impairment and anxiety behaviors induced by S-DEP. PGRN treatment also restored dendritic spine density in the hippocampus CA1 region and neurogenesis in hippocampus dentate gyrus (DG). These results indicate that an imbalance between TNFα and PGRN contributes to memory impairment and thigmotaxis/anxiety caused by sleep deprivation.
Highlights
Sleep disorder is becoming a widespread problem in current society, and is associated with impaired cognition and emotional disorders
Sleep is critical for learning and memory, and sleep deprivation (S-DEP) is detrimental to learning, brain maturation, and waking consciousness[1,2]
We find that S-DEP induces the over-expression of TNFα,but down-regulates PGRN expression in the hippocampus
Summary
Sleep disorder is becoming a widespread problem in current society, and is associated with impaired cognition and emotional disorders. Progranulin (PGRN), known as granulin epithelin precursor, promotes neurite outgrowth and cell survival, and is encoded by the GRN gene It is a tumor necrosis factor α receptor (TNFR) ligand which is implicated in many central nervous system diseases. PGRN treatment restored dendritic spine density in the hippocampus CA1 region and neurogenesis in hippocampus dentate gyrus (DG) These results indicate that an imbalance between TNFα and PGRN contributes to memory impairment and thigmotaxis/anxiety caused by sleep deprivation. S-DEP impairs the physiological and behavioral development through the dysregulation of microglial pro- and anti-inflammatory cytokines[7], such as tumor necrosis factor α(TNFα)[8]. The exact role of TNFα/PGRN balance in S-DEP-induced memory impairment remains unclear
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