scholarly journals 1800 MHz Radiofrequency Electromagnetic Field Impairs Neurite Outgrowth Through Inhibiting EPHA5 Signaling

2021 ◽  
Vol 9 ◽  
Author(s):  
Chunhai Chen ◽  
Qinglong Ma ◽  
Ping Deng ◽  
Min Lin ◽  
Peng Gao ◽  
...  
Keyword(s):  
Neurite Outgrowth ◽  
Camp Response Element Binding ◽  
Eph Receptors ◽  
Branch Points ◽  
Inhibitory Effects ◽  
Camp Response Element ◽  
Element Binding Protein ◽  
Neurite Development ◽  
The Brain ◽  
Radiofrequency Electromagnetic Field

The increasing intensity of environmental radiofrequency electromagnetic fields (RF-EMF) has increased public concern about its health effects. Of particular concern are the influences of RF-EMF exposure on the development of the brain. The mechanisms of how RF-EMF acts on the developing brain are not fully understood. Here, based on high-throughput RNA sequencing techniques, we revealed that transcripts related to neurite development were significantly influenced by 1800 MHz RF-EMF exposure during neuronal differentiation. Exposure to RF-EMF remarkably decreased the total length of neurite and the number of branch points in neural stem cells-derived neurons and retinoic acid-induced Neuro-2A cells. The expression of Eph receptors 5 (EPHA5), which is required for neurite outgrowth, was inhibited remarkably after RF-EMF exposure. Enhancing EPHA5 signaling rescued the inhibitory effects of RF-EMF on neurite outgrowth. Besides, we identified that cAMP-response element-binding protein (CREB) and RhoA were critical downstream factors of EPHA5 signaling in mediating the inhibitory effects of RF-EMF on neurite outgrowth. Together, our finding revealed that RF-EMF exposure impaired neurite outgrowth through EPHA5 signaling. This finding explored the effects and key mechanisms of how RF-EMF exposure impaired neurite outgrowth and also provided a new clue to understanding the influences of RF-EMF on brain development.

Occurrence of a transcription factor, cAMP response element-binding protein (CREB), in the postsynaptic sites of the brain

1998 ◽  
Vol 61 (1-2) ◽  
pp. 69-77 ◽  
Author(s):  
Tatsuo Suzuki ◽  
Nobuteru Usuda ◽  
Hiroshi Ishiguro ◽  
Shigehisa Mitake ◽  
Toshiharu Nagatsu ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Binding Protein ◽  
Camp Response Element Binding ◽  
Camp Response Element ◽  
Response Element ◽  
Element Binding Protein ◽  
The Brain

scholarly journals Neuroprotective Effect and Molecular Mechanism of [6]-Gingerol against Scopolamine-Induced Amnesia in C57BL/6 Mice

2018 ◽  
Vol 2018 ◽  
pp. 1-11 ◽  
Author(s):  
Chang-Yul Kim ◽  
Yongtaek Seo ◽  
Chan Lee ◽  
Gyu Hwan Park ◽  
Jung-Hee Jang
Keyword(s):  
Escape Latency ◽  
Neuroprotective Effect ◽  
Camp Response Element Binding ◽  
Behavior Changes ◽  
Camp Response Element ◽  
Memory Impairments ◽  
Maze Test ◽  
Y Maze ◽  
Element Binding Protein ◽  
The Brain

We have investigated the neuroprotective and memory enhancing effect of [6]-gingerol (GIN), a pungent ingredient of ginger, using an animal model of amnesia. To determine the neuroprotective effect of GIN on cognitive dysfunction, scopolamine (SCO, 1 mg/kg, i.p.) was injected into C57BL/6 mice, and a series of behavioral tests were conducted. SCO-induced behavior changes and memory impairments, such as decreased alteration (%) in Y-maze test, increased mean escape latency in water maze test, diminished step-through latency in passive avoidance test, and shortened freezing time in fear condition test, were significantly prevented and restored by the oral administration of GIN (10 or 25 mg/kg/day). To further verify the neuroprotective mechanism of GIN, we have focused on the brain-derived neurotrophic factor (BDNF). The administration of GIN elevated the protein expression of BDNF, which was mediated via the activation of protein kinase B/Akt- and cAMP-response element binding protein (CREB) signaling pathway. These results suggest that GIN may have preventive and/or therapeutic potentials in the management of memory deficit and cognitive impairment in mice with amnesia.

scholarly journals Acupuncture Activates ERK-CREB Pathway in Rats Exposed to Chronic Unpredictable Mild Stress

2013 ◽  
Vol 2013 ◽  
pp. 1-7 ◽  
Author(s):  
Jun Lu ◽  
Jia Liang ◽  
Jun-Ren Wang ◽  
Li Hu ◽  
Ya Tu ◽  
...  
Keyword(s):  
Camp Response Element Binding ◽  
Mild Stress ◽  
Chronic Unpredictable Mild Stress ◽  
Camp Response Element ◽  
Protein Levels ◽  
Extracellular Signal ◽  
Element Binding Protein ◽  
Phosphorylated Creb ◽  
The Brain ◽  
Creb Pathway

Extracellular signal-regulated kinase (ERK)-cAMP response element binding protein (CREB) signal pathway has been implicated in the pathogenesis of depression. There is growing evidence that acupuncture in traditional Chinese medicine has antidepressant-like effect. However, the effect of acupuncture on ERK-CREB pathway remains unknown. In our study, the antidepressant-like effect of acupuncture treatment was measured by sucrose intake test and open field test in rats exposed to chronic unpredictable mild stress (CUMS) for 4 weeks. The protein levels of ERK1/2, CREB, phosphorylated ERK1/2 (p-ERK1/2), and phosphorylated CREB (p-CREB) in the hippocampus (HP) and prefrontal cortex (PFC) were examined by Western blot analysis. Our results showed that CUMS rats exhibited the reduction in behavioral activities, whereas acupuncture stimulation at acupoints Baihui (Du20) and Neiguan (PC6) reversed the behavioral deficit. In addition, exposure to CUMS resulted in the decrease of p-ERK1/2 and p-CREB in the HP and PFC. Acupuncture increased the ratio of p-ERK1/2 to ERK1/2 and the ratio of p-CREB to CREB in the HP and PFC. Our study suggested that one potential way, by which acupuncture had antidepressant-like effect, might be mediated by activating the ERK-CREB pathway in the brain.

scholarly journals Insulin-Induced Cardiomyocytes Hypertrophy That Is Prevented by Taurine via β-alanine-Sensitive Na+-Taurine Symporter

Nutrients ◽  
2021 ◽  
Vol 13 (11) ◽  
pp. 3686
Author(s):  
Ashley Jazzar ◽  
Danielle Jacques ◽  
Ghassan Bkaily
Keyword(s):  
Essential Amino Acid ◽  
Camp Response Element Binding ◽  
Cardiomyocyte Hypertrophy ◽  
Camp Response Element ◽  
Ventricular Cardiomyocytes ◽  
Element Binding Protein ◽  
Taurine Treatment ◽  
Pre Treatment ◽  
The Brain

Although insulin-induced cardiac hypertrophy is reported, very little information is available on the hypertrophic effect of insulin on ventricular cardiomyocytes and the regulation of sodium and calcium homeostasis. Taurine is a non-essential amino acid synthesized by cardiomyocytes and the brain and is present in low quantities in many foods, particularly seafood. The purpose of this study was to investigate whether chronic exposure to insulin induces hypertrophy of ventricular cardiomyocytes that are associated with changes in Na+ and Ca2+ homeostasis and whether taurine pre-treatment prevents these effects. Our results showed that chronic treatment with insulin leads to cardiomyocyte hypertrophy that is associated with an increase in basal intracellular Na+ and Ca2+ levels. Furthermore, long-term taurine treatment prevents morphological and ionic remodeling induced by insulin. In addition, blocking the Na+-taurine co-transporter prevented the taurine antihypertrophic effect. Finally, the insulin-induced remodeling of cardiomyocytes was associated with a decrease in the ratio of phospho-CREB (pCREB) to total cAMP response element binding protein (CREB); taurine prevented this effect. In conclusion, our results show that insulin induces ventricular cardiomyocyte hypertrophy via downregulation of the pCREB/tCREB level and that chronic taurine treatment prevents this effect.

scholarly journals 2-Phenylethylamine (PEA) Ameliorates Corticosterone-Induced Depression-Like Phenotype via the BDNF/TrkB/CREB Signaling Pathway

2020 ◽  
Vol 21 (23) ◽  
pp. 9103
Author(s):  
Young-Ju Lee ◽  
Hye Ryeong Kim ◽  
Chang Youn Lee ◽  
Sung-Ae Hyun ◽  
Moon Yi Ko ◽  
...  
Keyword(s):  
Mouse Model ◽  
Signaling Pathway ◽  
Dendritic Spine ◽  
Hippocampal Neurons ◽  
Camp Response Element Binding ◽  
Medical Illness ◽  
Camp Response Element ◽  
Antidepressant Effects ◽  
Element Binding Protein ◽  
The Brain

Depression is a serious medical illness that is one of the most prevalent psychiatric disorders. Corticosterone (CORT) increases depression-like behavior, with some effects on anxiety-like behavior. 2-Phenethylamine (PEA) is a monoamine alkaloid that acts as a central nervous system stimulant in humans. Here, we show that PEA exerts antidepressant effects by modulating the Brain-derived neurotrophic factor (BDNF)/tropomyosin receptor kinase B (TrkB)/cAMP response element binding protein (CREB) signaling pathway in CORT-induced depression. To investigate the potential effects of PEA on CORT-induced depression, we first treated CORT (50 μM)-induced hippocampal neurons with 100 μM PEA for 24 h. We found that treatment with CORT altered dendritic spine architecture; however, treatment with PEA rescued dendritic spine formation via regulation of BDNF/TrkB/CREB signaling. Next, we used a mouse model of CORT-induced depression. Mice were treated with CORT (20 mg/kg) for 21 days, followed by assessments of a battery of depression-like behaviors. During the final four days of CORT exposure, the mice were treated with PEA (50 mg/kg). We found that CORT injection promoted depression-like behavior and significantly decreased BDNF and TrkB expression in the hippocampus. However, treatment with PEA significantly ameliorated the behavioral and biochemical changes induced by CORT. Our findings reveal that PEA exerts antidepressant effects by modulating the BDNF/TrkB/CREB signaling pathway in a mouse model of CORT-induced depression.

scholarly journals Does Aerobic and Resistance Exercise Influence Episodic Memory through Unique Mechanisms?

2020 ◽  
Vol 10 (12) ◽  
pp. 913
Author(s):  
Paul D. Loprinzi ◽  
Damien Moore ◽  
Jeremy P. Loenneke
Keyword(s):  
Episodic Memory ◽  
Resistance Exercise ◽  
Memory Function ◽  
Camp Response Element Binding ◽  
Anaerobic Exercise ◽  
Camp Response Element ◽  
Neural Modulation ◽  
Neural Communication ◽  
Element Binding Protein ◽  
The Brain

Aerobic and resistance exercise (acute and chronic) independently and collectively induce beneficial responses in the brain that may influence memory function, including an increase in cerebral blood flow, neurogenesis, neuroelectrical alterations, and protein production. However, whether aerobic and resistance exercise improve memory via similar or distinct mechanisms has yet to be fully explained. Here, we review the unique influence of aerobic and resistance exercise on neural modulation, proteins, receptors, and ultimately, episodic memory. Resistance training may optimize neural communication, information processing and memory encoding by affecting the allocation of attentional resources. Moreover, resistance exercise can reduce inflammatory markers associated with neural communication while increasing peripheral and central BDNF (brain-derived neurotrophic factor) production. Aerobic training increases hippocampal levels of BDNF and TrkB (Tropomyosin receptor kinase B), protein kinases and glutamatergic proteins. Likewise, both aerobic and anaerobic exercise can increase CREB (cAMP response element-binding protein) phosphorylation. Thus, we suggest that aerobic and resistance exercise may influence episodic memory via similar and, potentially, distinct mechanisms.

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