Abstract
Accumulating evidence suggests that sleep deprivation (S-Dep) is a critical risk factor for depression. Electroacupuncture (EA) treatment has been reported to ameliorate posttraumatic stress disorder- (PSTD-) like behavior and enhance hippocampal neurogenesis. However, whether EA treatment has any beneficial effect on S-Dep-induced depression-like behavior is still unknown. In the present study, we focused on whether EA at Baihui (GV20) can ameliorate the deterioration effect of S-Dep in mice. Mice were randomly divided into normal, S-Dep, S-Dep + EA, and S-Dep + sham EA groups. Cognitive behavior test and in vitro assay were performed separately to avoid the influence of behavior test on synaptic transmission and protein expression. Depression-like behaviors were determined by forced swimming test (FST), tail suspension test (TST), and Morris water maze (MWM). Neurogenesis was identified by BrdU, DCX, and NeuN immunofluorescence staining. In vitro long-term potentiation was detected by high frequency stimulation (HFS) at Schaffer collateral-CA1 synapses in hippocampal slices. Brain-derived neurotropic factor (BDNF) and tropomyosin receptor kinase B (TrkB) protein expression level were assayed by western blot. Our results indicated that D-Sep mice demonstrated depression-like behaviors determined by prolonged immobility duration in FST and TST; D-Sep mice also manifested spatial memory retention deficit in MWM. Furthermore, EA treatment ameliorated D-Sep-induced depression-like behaviors and spatial memory retention deficit. Mechanically, EA treatment alleviated neuron progenitor cell proliferation and differentiation, ameliorated the field excitatory postsynaptic potentials (fEPSPs) slope impaired by S-Dep, and elevated BDNF/TrkB protein expression. Taken together, our data suggested that EA treatment has a protective effect on S-Dep-induced depression-like behavior and cognitive impairment, which may be through regulating BDNF/TrkB protein expression.
Highlights
Sleep, which has been discovered as a state of consolidation of newly formulated memory, is crucial for learning new information and mental performance [1]
forced swimming test (FST) and TST were both classic behavior test models for depression-like symptoms. e immobility time in FST was markedly elevated in sleep deprivation (S-Dep) group (121.50 ± 8. 94 s) compared with normal group (76.56 ± 7. 12 s), which was reversed by EA treatment (81.35 ± 6. 95 s)
Stimulation at GV20 located at the top of the head is widely accepted for the cure of neuropsychiatric disorders in the clinical practice, the underlying molecular mechanism is controversial. e current study uses a mice model of sleep deprivation to investigate the potential mechanism of EA at GV20 acupoints on cognitive impairment
Summary
Sleep, which has been discovered as a state of consolidation of newly formulated memory, is crucial for learning new information and mental performance [1]. Sleep loss or insomnia has been proven to contribute to hippocampaldependent cognition deficits and depression-like behavior; the underlying mechanisms include disruption of synaptic plasticity at electrophysiology and molecular levels as well as at a structural level [2]. Long time potentiation (LTP) is a form of synaptic plasticity adopted as an in vitro biological model of learning and memory. Ample evidence has demonstrated that sleep deprivation can have detrimental effects on memory formation and LTP induction [3,4,5]. BDNF, a member of the neurotrophin family, is a significant modulator in synaptic plasticity and memory formation. BDNF needs to bind to its high-affinity protein kinase receptor, TrkB, to exhibit its biological effect [6]
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