Electroacupuncture Improves Synaptic Function in SAMP8 Mice Probably via Inhibition of the AMPK/eEF2K/eEF2 Signaling Pathway

• Published in: Evidence-based complementary and alternative medicine 2019, Vol.2019 (2019), p.1-10
• Main Authors: Lin, Ruhui, Lin, Lan, Wang, Feng, Qian, Changhui, Guo, Wanqing, Li, Feifei, Yang, Wendan, Dong, Weiguo, Li, Changzhen
• Format: Article
• Language: English
• Subjects: Acupuncture; Advertising executives; Alzheimer's disease; AMP; AMP-activated protein kinase; Animal cognition; Brain research; Cognitive ability; Disease; Electroacupuncture; Elongation; Evidence-based medicine; Gene expression; Health aspects; Immunohistochemistry; Kinases; Laboratory animals; Medicine; Memory; Microscopy; Neurodegeneration; Neurosciences; Polymerase chain reaction; Postsynaptic density; Postsynaptic density proteins; Protein kinases; Protein structure; Protein synthesis; Proteins; RNA; Senescence; Signal transduction; Synapses; Synaptic plasticity; Synaptophysin; Transgenic animals; Transmission electron microscopy; Vertebrae
• ISSN: 1741-427X; 1741-4288
• DOI: 10.1155/2019/8260815

Synaptic loss and dysfunction is associated with cognitive impairment in Alzheimer’s disease (AD). Recent evidence indicates that the AMP-activated protein kinase (AMPK)/eukaryotic elongation factor-2 kinase (eEF2K)/eukaryotic elongation factor-2 (eEF2) pathway was implicated in synaptic plasticity in AD. Therapeutic strategies for AD treatment are currently limited. Here, we investigate the effects of electroacupuncture (EA) on synaptic function and the AMPK/eEF2K/eEF2 signaling pathway in male senescence-accelerated mouse-prone 8 (SAMP8) mice. Male 7-month-old SAMP8 and SAMR1 mice (senescence-accelerated mouse resistant 1) were randomly divided into 3 groups: SAMR1 control group (Rc), SAMP8 control group (Pc), and SAMP8 electroacupuncture group (Pe). The Pe group was treated with EA for 30 days. Transmission electron microscopy (TEM) was used to observe the structure of synapse. The protein and mRNA expression of synaptophysin (SYN) and postsynaptic density 95 (PSD95) was examined by immunohistochemistry, western blot, and real-time RT-PCR. The activity of AMPK and eEF2K was studied by western blot. Our results showed that EA ameliorated synaptic loss, increased the expression of SYN and PSD95, and inhibited AMPK activation and eEF2K activity. Collectively, these findings suggested that the mechanisms of EA improving synaptic function in AD may be associated with the inhibition of the AMPK/eEF2K/eEF2 signaling pathway.