The purpose of this study is to investigate the mechanism of alternative responses to low dose irradiation for neuronal cell proliferation in the dentate gyrus of rats. To determine the effect of a single exposure to radiation, rats were irradiated with a single dose of 0.1, 1, 10 or 20 Gy. To determine the effect of the cumulative dose, the animals were irradiated daily with 0.01 Gy or 0.1 Gy from 1 to 4 days. The neuronal cell proliferation was evaluated using immunohistochemistry for 5-bromo-2'-deoxyuridine (BrdU), Ki-67 and terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling (TUNEL) staining. Four consecutive daily irradiations with a 0.01 Gy/fraction increased the number of BrdU-positive and Ki-67-positive cells in a dose dependent manner, but this did not affect the number of TUNEL-positive cells. However, there was not a dose dependent relationship for the 0.1 Gy/fraction irradiation with the number of BrdU, Ki-67 and TUNEL positive cells. Our data support the explanation that the adaptive response, induced by low-dose radiation, in the hippocampus of rats is more likely a reflection of the perturbations of cell cycle progression.
Rats, Sprague-Dawley ; Rats ; Radiation Dosage ; Neurons/*cytology/*radiation effects ; Neuronal Plasticity/*radiation effects ; Male ; Dose-Response Relationship, Radiation ; Dentate Gyrus/*cytology/*radiation effects ; Cell Survival/radiation effects ; Cell Proliferation/*drug effects ; Animals ; Adaptation, Physiological/radiation effects

OBJECTIVEThe aim of this study is to investigate whether microwave exposure would affect the N-methyl-D-aspartate receptor (NMDAR) signaling pathway to establish whether this plays a role in synaptic plasticity impairment.

METHODS48 male Wistar rats were exposed to 30 mW/cm2 microwave for 10 min every other day for three times. Hippocampal structure was observed through H&E staining and transmission electron microscope. PC12 cells were exposed to 30 mW/cm2 microwave for 5 min and the synapse morphology was visualized with scanning electron microscope and atomic force microscope. The release of amino acid neurotransmitters and calcium influx were detected. The expressions of several key NMDAR signaling molecules were evaluated.

RESULTSMicrowave exposure caused injury in rat hippocampal structure and PC12 cells, especially the structure and quantity of synapses. The ratio of glutamic acid and gamma-aminobutyric acid neurotransmitters was increased and the intracellular calcium level was elevated in PC12 cells. A significant change in NMDAR subunits (NR1, NR2A, and NR2B) and related signaling molecules (Ca2+/calmodulin-dependent kinase II gamma and phosphorylated cAMP-response element binding protein) were examined.

CONCLUSION30 mW/cm2 microwave exposure resulted in alterations of synaptic structure, amino acid neurotransmitter release and calcium influx. NMDAR signaling molecules were closely associated with impaired synaptic plasticity.

Animals ; Gene Expression Regulation ; radiation effects ; Hippocampus ; cytology ; Microwaves ; Neuronal Plasticity ; radiation effects ; Neurons ; radiation effects ; Neurotransmitter Agents ; metabolism ; PC12 Cells ; Rats ; Receptors, N-Methyl-D-Aspartate ; genetics ; metabolism ; Signal Transduction ; physiology ; radiation effects ; Time Factors

Animals ; Calcium-Calmodulin-Dependent Protein Kinase Type 2 ; genetics ; metabolism ; Cyclic AMP Response Element-Binding Protein ; genetics ; metabolism ; Male ; MicroRNAs ; radiation effects ; Microwaves ; adverse effects ; Neuronal Plasticity ; radiation effects ; Random Allocation ; Rats ; Rats, Wistar ; Receptors, N-Methyl-D-Aspartate ; genetics ; metabolism