Reduction of Phosphorylated Synapsin I (Ser-553) Leads to Spatial Memory Impairment by Attenuating GABA Release after Microwave Exposure in Wistar Rats

Abstract

BackgroundAbnormal release of neurotransmitters after microwave exposure can cause learning and memory deficits. This study investigated the mechanism of this effect by exploring the potential role of phosphorylated synapsin I (p-Syn I).MethodsWistar rats, rat hippocampal synaptosomes, and differentiated (neuronal) PC12 cells were exposed to microwave radiation for 5 min at a mean power density of 30 mW/cm2. Sham group rats, synaptosomes, and cells were otherwise identically treated and acted as controls for all of the following post-exposure analyses. Spatial learning and memory in rats was assessed using the Morris Water Maze (MWM) navigation task. The protein expression and presynaptic distribution of p-Syn I and neurotransmitter transporters were examined via western blotting and immunoelectron microscopy, respectively. Levels amino acid neurotransmitter release from rat hippocampal synaptosomes and PC12 cells were measured using high performance liquid chromatograph (HPLC) at 6 hours after exposure, with or without synapsin I silencing via shRNA transfection.ResultsIn the rat experiments, there was a decrease in spatial memory performance after microwave exposure. The expression of p-Syn I (ser-553) was decreased at 3 days post-exposure and elevated at later time points. Vesicular GABA transporter (VGAT) was significantly elevated after exposure. The GABA release from synaptosomes was attenuated and p-Syn I (ser-553) and VGAT were both enriched in small clear synaptic vesicles, which abnormally assembled in the presynaptic terminal after exposure. In the PC12 cell experiments, the expression of p-Syn I (ser-553) and GABA release were both attenuated at 6 hours after exposure. Both microwave exposure and p-Syn I silencing reduced GABA release and maximal reduction was found for the combination of the two, indicating a synergetic effect.Conclusionp-Syn I (ser-553) was found to play a key role in the impaired GABA release and cognitive dysfunction that was induced by microwave exposure.

High salt diet impairs memory‐related synaptic plasticity via increased oxidative stress and suppressed synaptic protein expression

“…Both SYS and SYP are associated with neurotransmitter release, and are responsible for the formation and anchoring of synaptic vesicles, as well as contributing to fast and efficient neurotransmission . A proportional relationship between the ability to remember and the synaptic vesicle proteins SYS and SYP was observed in many previous studies . Recent studies on rats also show that a systemic increase in plasma Na+ can stimulate some neurosecretory cells to release BDNF , and that BDNF is associated with the abolishment of GABAergic signaling inhibition due to a chronic HS intake, thereby suggesting that dietary salt can affect neurotrophin‐induced plasticity .…”

Study on dose-dependent, frequency-dependent, and accumulative effects of 1.5 GHz and 2.856 GHz microwave on cognitive functions in Wistar rats

“…It was reported that microwave could induce the impairment in learning and memory functions, brain electric activities, and brain structures 5 – 7 . Besides, many studies were made to test the health hazards of microwave and the nervous system was believed very sensitive to microwave exposure 8 . Study showed that the microwaves induced biological effects were related with their power densities, frequencies, waveforms, modulation and durations of exposure 9 .…”

Cross-talk between microglia and neurons regulates HIV latency

“…To maximize HIV expression, the HC69 cells were pre-treated with TNF-α or poly (I:C), a TLR3 agonist that mimics the effects of circulating bacterial rRNA and potently induces HIV by activation of IRF3 [37]. High levels of expression of α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor (AMPA receptor) [116][117][118], increased the phosphorylation of MAP2 (p-MAP2) [119,120] and decreased phosphorylated synapsin I (p-synapsin) [121], which are both associated with neurodegeneration. Analysis of representative western blots showed no statistically significant (N.S.)…”