OBJECTIVETo determine the threshold of millimeter wave irradiation for fetal injury in mice and the mechanism of decrease of learning and memory function in their offsprings and to verify whether the millimeter wave has the non-thermal effect.

METHODSPregnant mice were irradiated by millimeter wave with frequencies of 37.4, 42.2, 53.0 and 60.0 GHz at power densities of 1, 3, 5, 8 mW/cm(2) for two hours daily from the 6th to 15th day of their gestation. Learning and memory functions of their offsprings were tested by a Y-type electric maze. c-Fos protein expression level in hippocampus of their offsprings was determined with immunohistochemistry 0, 30, 60, 90 and 120 minutes after the offsprings were trained respectively.

RESULTSThe minimal power density of millimeter wave for the decrease in learning and memory function and decrease of c-Fos protein expression level in hippocampus of their offsprings caused by 37.4, 42.2 GHz and 53.0, 60.0 GHz was 5 and 3 mW/cm(2). Severity of injury for learning and memory in offsprings caused by irradiation increased with the power density of millimeter wave. The millimeter wave did not cause increase of the body temperature of the pregnant mice.

CONCLUSIONThe threshold of millimeter wave with 37.4, 42.2 GHz, and 53.0, 60.0 GHz causing fetal injury in mice is 5 and 3 mW/cm(2) respectively. The decrease in learning and memory functions in offspring mice is related with decrease of c-Fos protein expression level in hippocampus. Millimeter wave has the non-thermal effects.

Animals ; Dose-Response Relationship, Radiation ; Female ; Hippocampus ; metabolism ; radiation effects ; Immunohistochemistry ; Learning ; radiation effects ; Memory ; radiation effects ; Mice ; Mice, Inbred BALB C ; Microwaves ; adverse effects ; Pregnancy ; Prenatal Exposure Delayed Effects ; Proto-Oncogene Proteins c-fos ; biosynthesis

OBJECTIVETo study the changes of morphology and function in rat hippocampus induced by high power microwave (HPM) radiation.

METHODSFifty male Wistar rats were radiated by HPM. Then their learning and memory abilities were tested with Y maze and were sacrificed 6 h, 1 d, 3 d and 7 d after radiation. The hippocampus was taken out to study the basic pathologic changes, apoptosis and the expressions of neuron-specific enolase (NSE) and glial fibrillary acidic protein (GFAP) by means of HE staining, Nissel body staining, in situ terminal end labeling and immunohistochemistry.

RESULTSThe learning and memory abilities of rats reduced significantly after HPM radiation. HPM also resulted in rarefaction, edema and hemangiectasia of hippocampus, nervous cells degeneration and necrosis, decrease or disappearance of Nissel bodies. The injuries were more serious in field CA4 and dentate gyrus, which showed dose-effect relationship, and were progressively aggravated within 7 days. The apoptosis cells were significantly increased. NSE was increased in neurons. The NSE positive areas were also seen in the interstitial matrix and blood vessels. GFAP was increased in astrocytes, which became shorter and thicker.

CONCLUSIONHPM can damage the abilities of learning and memory and results in morphologic changes in hippocampus. The major pathologic changes are degeneration, apoptosis and necrosis of neurons and edema in interstitium. NSE and GFAP play an important role in the pathologic process.

Animals ; Apoptosis ; radiation effects ; Glial Fibrillary Acidic Protein ; metabolism ; Hippocampus ; metabolism ; pathology ; radiation effects ; Learning ; radiation effects ; Male ; Memory ; radiation effects ; Microwaves ; adverse effects ; Phosphopyruvate Hydratase ; metabolism ; Rats ; Rats, Wistar

OBJECTIVETo gain a better understanding of gene expression changes in the brain following microwave exposure in mice. This study hopes to reveal mechanisms contributing to microwave-induced learning and memory dysfunction.

METHODSMice were exposed to whole body 2100 MHz microwaves with specific absorption rates (SARs) of 0.45 W/kg, 1.8 W/kg, and 3.6 W/kg for 1 hour daily for 8 weeks. Differentially expressing genes in the brains were screened using high-density oligonucleotide arrays, with genes showing more significant differences further confirmed by RT-PCR.

RESULTSThe gene chip results demonstrated that 41 genes (0.45 W/kg group), 29 genes (1.8 W/kg group), and 219 genes (3.6 W/kg group) were differentially expressed. GO analysis revealed that these differentially expressed genes were primarily involved in metabolic processes, cellular metabolic processes, regulation of biological processes, macromolecular metabolic processes, biosynthetic processes, cellular protein metabolic processes, transport, developmental processes, cellular component organization, etc. KEGG pathway analysis showed that these genes are mainly involved in pathways related to ribosome, Alzheimer's disease, Parkinson's disease, long-term potentiation, Huntington's disease, and Neurotrophin signaling. Construction of a protein interaction network identified several important regulatory genes including synbindin (sbdn), Crystallin (CryaB), PPP1CA, Ywhaq, Psap, Psmb1, Pcbp2, etc., which play important roles in the processes of learning and memorye.

CONCLUSIONLong-term, low-level microwave exposure may inhibit learning and memory by affecting protein and energy metabolic processes and signaling pathways relating to neurological functions or diseases.

Animals ; Computational Biology ; Gene Expression ; radiation effects ; Learning ; Memory ; Mice ; Microwaves ; Reverse Transcriptase Polymerase Chain Reaction

OBJECTIVE: To estimate the detrimental effects of shortwave exposure on rat hippocampal structure and function and explore the underlying mechanisms. METHODS: One hundred Wistar rats were randomly divided into four groups (25 rats per group) and exposed to 27 MHz continuous shortwave at a power density of 5, 10, or 30 mW/cm2 for 6 min once only or underwent sham exposure for the control. The spatial learning and memory, electroencephalogram (EEG), hippocampal structure and Nissl bodies were analysed. Furthermore, the expressions of N-methyl-D-aspartate receptor (NMDAR) subunits (NR1, NR2A, and NR2B), cAMP responsive element-binding protein (CREB) and phosphorylated CREB (p-CREB) in hippocampal tissue were analysed on 1, 7, and 14 days after exposure. RESULTS: The rats in the 10 and 30 mW/cm2 groups had poor learning and memory, disrupted EEG oscillations, and injured hippocampal structures, including hippocampal neurons degeneration, mitochondria cavitation and blood capillaries swelling. The Nissl body content was also reduced in the exposure groups. Moreover, the hippocampal tissue in the 30 mW/cm2 group had increased expressions of NR2A and NR2B and decreased levels of CREB and p-CREB. CONCLUSION Shortwave exposure (27 MHz, with an average power density of 10 and 30 mW/cm2) impaired rats' spatial learning and memory and caused a series of dose-dependent pathophysiological changes. Moreover, NMDAR-related CREB pathway suppression might be involved in shortwave-induced structural and functional impairments in the rat hippocampus.
Animals ; Cyclic AMP Response Element-Binding Protein ; genetics ; metabolism ; Dose-Response Relationship, Radiation ; Electroencephalography ; radiation effects ; Hippocampus ; radiation effects ; Male ; Memory ; radiation effects ; Nissl Bodies ; physiology ; radiation effects ; Radio Waves ; adverse effects ; Random Allocation ; Rats ; Rats, Wistar ; Receptors, N-Methyl-D-Aspartate ; genetics ; metabolism ; Spatial Learning ; radiation effects

Object recognition memory and contextual fear conditioning task performance in adult C57BL/6 mice exposed to cranial fast neutron irradiation (0.8 Gy) were examined to evaluate hippocampus-related behavioral dysfunction following acute exposure to relatively low doses of fast neutrons. In addition, hippocampal neurogenesis changes in adult murine brain after cranial irradiation were analyzed using the neurogenesis immunohistochemical markers Ki-67 and doublecortin (DCX). In the object recognition memory test and contextual fear conditioning, mice trained 1 and 7 days after irradiation displayed significant memory deficits compared to the sham-irradiated controls. The number of Ki-67- and DCX-positive cells decreased significantly 24 h post-irradiation. These results indicate that acute exposure of the adult mouse brain to a relatively low dose of fast neutrons interrupts hippocampal functions, including learning and memory, possibly by inhibiting neurogenesis.
Animals ; Cranial Irradiation ; *Fast Neutrons ; Hippocampus/metabolism/physiology/*radiation effects ; Immunohistochemistry ; Ki-67 Antigen/metabolism ; Male ; Memory/physiology/*radiation effects ; Mice ; Mice, Inbred C57BL ; Microtubule-Associated Proteins/metabolism ; Neurogenesis/physiology/*radiation effects ; Neuropeptides/metabolism

OBJECTIVETo investigate the effect of cerebral X-ray irradiation on learning and memory function in young rats.

METHODSFifty-four SD rats aged 35 d were randomly divided into 3 groups with 18 in each group: rats in 3-d group and 7-d group received X-ray irradiation with a dose of 28.5 mGy/d for 3 d and 7 d, respectively; rats in control group received sham X-ray irradiation. Morris water maze (MWM) was tested when animals at age of 60 d; then the animals were sacrificed and brain samples were taken. The neurodegeneration was observed by Fluro-Jade B staining; the expression of N-methyl-aspartate (NMDA) receptors subunit 2B (NR2B) and postsynaptic density protein-95 (PSD-95) in the hippocampus were analyzed by immunofluorescence and Western blot methods, respectively, and ultrastructure of CA1 region was observed with electron microscopy.

RESULTSNo significant difference in 1-4 d escape latency as shown in MWM test was noted between 3d group and control group (P>0.05); while the escape latency in 7d group was significantly longer than that in control group (P<0.01). No significant differences in lingering in the quadrant and the frequency of passing through the original platform between 3-d group and control group (P>0.05), while those in 7-d group were significantly lower than those in control group (P<0.01). Compared to control group, the number of FJB positive cells in 7-d group was increased (P<0.01); the expressions of NR2B and PSD-95 in hippocampus CA1 region were also increased (P<0.05). The ultrastructure observation in 7-d group showed that the synapse structure of some neurons was impaired.

CONCLUSIONX-ray irradiation may affect learning and memory function of young rats, which is associated with overexpression of NR2B and PSD-95 in hippocampal regions.

Animals ; Brain ; radiation effects ; CA1 Region, Hippocampal ; metabolism ; radiation effects ; Disks Large Homolog 4 Protein ; Intracellular Signaling Peptides and Proteins ; metabolism ; Learning ; radiation effects ; Membrane Proteins ; metabolism ; Memory ; radiation effects ; Neurons ; Rats ; Rats, Sprague-Dawley ; Receptors, N-Methyl-D-Aspartate ; metabolism ; Synapses ; X-Rays

OBJECTIVETo analyze the effects of long-term microwave exposure on hippocampal structure and function in the rat.

METHODSExperiments were performed on 184 male Wistar rats (three exposure groups and a sham group). Microwaves were applied daily for 6 min over 1 month at average power densities of 2.5, 5, and 10 mW/cm2. Learning and memory abilities were assessed by Morris water maze. High performance liquid chromatography was used to detect neurotransmitter concentrations in the hippocampus. Hippocampal structures were observed by histopathological analysis.

RESULTSFollowing long-term microwave exposure there was a significant decrease in learning and memory activity in the 7 d, 14 d, and 1 m in all three microwave exposure groups. Neurotransmitter concentrations of four amino acids (glutamate, aspartic acid, glycine, and gamma-aminobutyric acid) in hippocampus were increased in the 2.5 and 5 mW/cm2 groups and decreased in the 10 mW/cm2 group. There was evidence of neuronal degeneration and enlarged perivascular spaces in the hippocampus in the microwave exposure groups. Further, mitochondria became swollen and cristae were disordered. The rough endoplasmic reticulum exhibited sacculated distension and there was a decrease in the quantity of synaptic vesicles.

CONCLUSIONThese data suggest that the hippocampus can be injured by long-term microwave exposure, which might result in impairment of cognitive function due to neurotransmitter disruption.

Animals ; Chromatography, High Pressure Liquid ; Cognition ; Hippocampus ; pathology ; physiopathology ; radiation effects ; Learning ; Male ; Memory ; Microscopy, Electron, Transmission ; Microwaves ; Rats ; Rats, Wistar

This study examined whether amifostine (WR-2721) could attenuate memory impairment and suppress hippocampal neurogenesis in adult mice with the relatively low-dose exposure of acute radiation syndrome (ARS). These were assessed using object recognition memory test, the terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling assay, and immunohistochemical markers of neurogenesis [Ki-67 and doublecortin (DCX)]. Amifostine treatment (214 mg/kg, i.p.) prior to irradiation significantly attenuated the recognition memory defect in ARS, and markedly blocked the apoptotic death and decrease of Ki-67- and DCX-positive cells in ARS. Therefore, amifostine may attenuate recognition memory defect in a relatively low-dose exposure of ARS in adult mice, possibly by inhibiting a detrimental effect of irradiation on hippocampal neurogenesis.
Acute Radiation Syndrome/drug therapy/*immunology/psychology ; Amifostine/*pharmacology/therapeutic use ; Animals ; Apoptosis/immunology ; Gamma Rays/*adverse effects ; Hippocampus/immunology ; Immunohistochemistry ; In Situ Nick-End Labeling ; Male ; Memory/*radiation effects ; Mice ; Mice, Inbred ICR ; Neurogenesis/immunology ; Radiation-Protective Agents/*pharmacology/therapeutic use