Alzheimer Disease/pathology* ; Animals ; C9orf72 Protein/metabolism* ; Mice ; Microglia/pathology* ; Neuronal Plasticity ; Neurons/pathology* ; Synapses/pathology*

OBJECTIVEThe relationship between selenium deficiency and the changes of synaptic structure in the CA3 area of hippocampus were studied in the third generation rats.

METHODSA selenium deficiency model was established by feeding rats with selenium-deficient food. The rats were divided into 4 groups: control (Se+I+), selenium deficiency (Se-I+), iodine deficiency (Se+I-), and both deficient group (Se-I-). The hippocampuses were dissected from the third generation rats on the 21st gestational day and the ultrastructural features of hippocampal synapses were observed with electron microscope. The length of active zone, synaptic curvatures, post-synaptic density (PSD) and synaptic cleft were quantitatively described.

RESULTSCompared with the control, the length of active zone and the thickness of PSD were significantly decreased in Se-I+, Se+I- and Se-I- groups [(261.7 +/- 50.1) nm, (286.7 +/- 41.6) nm and (220.8 +/- 61.6) nm contrast to (312.4 +/- 47.7) nm, P < 0.01], so were the synaptic curvatures in Se-I+, Se+I- and Se-I- groups [(22.9 +/- 6.3) nm, (27.5 +/- 8.6) nm and (25.2 +/- 6.5) nm contrast to (48.1 +/- 12.3) nm, P < 0.01]; the width of synaptic cleft were also decreased significantly in Se-I- [(11.1 +/- 3.3) nm contrast to (16.1 +/- 4.0) nm, P < 0.01].

CONCLUSIONSelenium deficiency might cause changes of neuronal functions at the synaptic level, and furthermore, affect learning and memory.

Animals ; Female ; Hippocampus ; pathology ; Iodine ; deficiency ; Male ; Rats ; Rats, Sprague-Dawley ; Selenium ; deficiency ; Synapses ; pathology ; ultrastructure

The present study investigated the effects of prenatal exposure to the magnetic resonance imaging (MRI) magnetic fields on the synaptic ultrastructure of hippocampal formation of rats at different postnatal development stages. Pregnant rats with gestation of 12-18 days were exposed to the magnetic fields used for MRI clinical applications. When the offspring were 1, 2, or 5-month-old, the synaptic morphologic parameters were measured in female offspring. In the 2-month-old MRI group, the curvature of synaptic interface, the length of active zone and the surface density per unit volume (S(v)) of active zone in the dentate gyrus (DG) decreased significantly, and the width of synaptic cleft increased in the CA1 area. In the 5-month-old MRI group, the width of synaptic cleft increased, the thickness of postsynaptic density and the curvature of synaptic interface decreased significantly in the CA1 region, and the width of synaptic cleft increased in the DG. No significant change was observed in the 1-month-old group. These results suggest that prenatal exposure to the medical magnetic fields causes synaptic ultrastructural changes. The relationship of these changes with behavioral impairments was discussed.
Animals ; Female ; Hippocampus ; pathology ; Magnetic Resonance Imaging ; adverse effects ; Pregnancy ; Prenatal Exposure Delayed Effects ; Rats ; Rats, Sprague-Dawley ; Synapses ; pathology

Adult ; Azoospermia/pathology* ; DNA Breaks, Double-Stranded ; DNA Repair ; Humans ; Infertility, Male/pathology* ; Male ; Prophase ; Prostate/pathology* ; Recombination, Genetic ; Synapses/pathology* ; Testis/pathology*

OBJECTIVE AND METHODSTo evaluate synaptic changes using synaptophysin immunohistochemstry in rat and mouse, which spinal cords were subjected to graded compression trauma at the level of Th8-9.

RESULTSNormal animals showed numerous fine dots of synaptophysin immunoreactivity in the gray matter. An increase in synaptophysin immunoreactivity was observed in the neuropil and synapses at the surface of motor neurons of the anterior horns in the Th8-9 segments lost immunoreactivity at 4-hour point after trauma. The immunoreactive synapses reappeared around motor neurons at 9-day point. Unexpected accumulation of synaptophysin immunoreactivity occurred in injured axons of the white matter of the compressed spinal cord.

CONCLUSIONSynaptic changes were important components of secondary injuries in spinal cord trauma. Loss of synapses on motor neurons may be one of the factors causing motor dysfunction of hind limbs and formation of new synapses may play an important role in recovery of motor function. Synaptophysin immunohistochemistry is also a good tool for studies of axonal swellings in spinal cord injuries.

Animals ; Axons ; metabolism ; pathology ; Female ; Immunohistochemistry ; Male ; Mice ; Mice, Inbred Strains ; Rats ; Rats, Sprague-Dawley ; Spinal Cord Compression ; Spinal Cord Injuries ; metabolism ; pathology ; Synapses ; metabolism ; pathology ; Synaptophysin ; metabolism

OBJECT: To investigate the changes in the expression_level of synaptophysin following diffuse brain injury (DBI) in rats and to correlate the changes of the synaptophysin expression_level with the post injury time interval. METHODS: Wister rats were used as a DBI model induced by Marmarou method. The changes of synaptophysin immunoreactivity on coronal sections of the rats sampled at different post-injury time intervals were used as a marker. The densitometry of the synaptophysin immunoreactivity was documented by imaging technique and analyzed by SPSS software. RESULTS: The expression level of synaptophysin in DBI rats showed dynamic changes following DBI as well as during the repairing period. CONCLUSION The changes of synaptophysin level may be used as a marker for estimation of the post injury time interval in DBI.
Animals ; Brain/pathology* ; Brain Injuries/pathology* ; Cerebral Cortex/pathology* ; Diffuse Axonal Injury/pathology* ; Disease Models, Animal ; Immunohistochemistry ; Intracranial Hemorrhage, Traumatic/pathology* ; Neurons/pathology* ; Rats ; Rats, Sprague-Dawley ; Staining and Labeling ; Synapses/pathology* ; Synaptophysin/metabolism* ; Time Factors

OBJECTIVETo observe the effects of hyperbaric oxygen (HBO) on synaptic ultrastructure and the synaptophysin expression (p38) in hippocampal CA3 after hypoxia-ischemic brain damage (HIBD) in neonatal rats.

METHODSThe rat model of HIBD was made by the method of Bjelke and divided randomly into two groups (n = 10)--HIBD group and HBO-treated HIBD group. Another 20 rats underwent sham-operation and were also divided randomly into HBO-treated control group and the control group. After 24 h of the operation, the rats of the HBO-treated groups received HBO (2ATA, 1 h/d) for 14 days. When rats were 4 weeks old, the learning-memory ability of rats in every group was evaluated through water-maze test. Their hippocampal ultrastructure was observed with electron microscope and the p38 expression was detected immunohistochemically.

RESULTSCompared with the control group [(10.6 +/- 3.4) times], the water-maze learning ability of the rats in HIBD group [(15.5 +/- 4.9) times] was significantly decreased (P < 0.01), while the learning-memory ability of the HBO-treated HIBD group [(11.3 +/- 2.6) times] was significantly improved. There was no significant difference in the water-maze test between the HBO-treated HIBD group and the control group (P > 0.05). Compared with the control group, the ultrastructure of pyramidal neuron of hippocampal CA3 was distorted in HIBD group under the electron microscope. Compared with that in HBO-treated HIBD group (0.77 +/- 0.17, 0.67 +/- 0.16, 0.46 +/- 0.13, 0.86 +/- 0.14) and the control group (0.82 +/- 0.16, 0.70 +/- 0.16, 0.53 +/- 0.15, 0.91 +/- 0.17), the corrected optical densities (COD) of immunoreactive products of the hippocampal CA3 p38 were significantly decreased in HIBD group (0.41 +/- 0.19, 0.21 +/- 0.11, 0.08 +/- 0.03, 0.38 +/- 0.16) (P < 0.01). There was no significant difference in either ultrastructure or immunohistochemically reactive COD of p38 between the HBO-treated HIBD group and the control group (P > 0.05).

CONCLUSIONUnderlying the induction of synaptic plasticity and reducing the ultrastructural damage may be involved in the mechanism of HBO in the brain rehabilitation in perinatal brain damage with hypoxia-ischemia.

Animals ; Animals, Newborn ; Female ; Hippocampus ; metabolism ; pathology ; Hyperbaric Oxygenation ; Hypoxia-Ischemia, Brain ; metabolism ; pathology ; therapy ; Pregnancy ; Rats ; Rats, Sprague-Dawley ; Synapses ; metabolism ; ultrastructure ; Synaptophysin ; metabolism

OBJECTIVETo investigate the effect of microwave radiation on synaptic structure, characteristic of synaptosome, the contents and release of neurotransmitters in hippocampus in Wistar rats.

METHODSWistar rats were exposed to microwave radiation with average power density of 30 mW/cm(2). Electron telescope was used to study the change of the synaptic structure at 6 h after radiation and to identify synaptosome. Flow cytometry and electron spin resonance were used to study the change of the concentration of Ca(2+) in synapse and the fluidity of membrane proteins of synaptosome. High performance liquid chromatography (HPLC) and spectrophotometer were used to study the changes of contents and release of amino acids and acetylcholine in hippocampus.

RESULTSMicrowave radiation of 30 mW/cm(2) caused deposits of synapse vesicle, elongation of active zone, the increase of thickness of postsynaptic density (PSD) and curvature, and perforation of synapse. The concentration of Ca(2+) in synapse (P<0.01) and tc of membrane proteins (P<0.01) of synaptosome increased contents of glutamic acid and glycine (P<0.01) and release of GABA increased the increase of contents and release of acetylcholine, and activity of acetyl cholinesterase (P<0.01) increased.

CONCLUSIONMicrowave radiation can induce the injure of synaptic structure and function of hippocampus, and then induce the disorder of the ability of learning and memory in rats.

Animals ; Hippocampus ; metabolism ; pathology ; radiation effects ; Male ; Microwaves ; adverse effects ; Rats ; Rats, Wistar ; Synapses ; metabolism ; pathology ; radiation effects ; Synaptosomes ; metabolism ; radiation effects

During the central nervous system (CNS) development, the interactions between intrinsic genes and extrinsic environment ensure that each neuronal developmental stage (eg. neuronal proliferation, differentiation, migration, axon extension, dendritogenesis and formation of functional synapses) occurs in the proper timing and sequence. The successful coordination requires that numerous groups of genes are exquisitely regulated in a spatiotemporal manner by various regulatory mechanisms, including sequence-specific DNA-binding proteins, histone modifications, DNA methylation, chromatin remodeling, and microRNAs (miRNAs). By targeting chromatin structure, transcription and translation processes, these mechanisms form a regulatory network to accomplish the fine regulation of gene expression in response to environmental stimuli at different developmental stages. Dysregulation of the gene expression during neuronal development has been shown to be implicated in a number of neurodevelopmental disorders, such as autism spectrum disorders (ASD), Rett syndrome (RTT), Fragile-X syndrome (FXS) and other genetic diseases. The further understanding of the regulation of gene expression during neuronal development may provide new approaches for the diagnosis and treatment of these disorders.
Cell Differentiation ; Child Development Disorders, Pervasive ; genetics ; DNA Methylation ; DNA-Binding Proteins ; Gene Expression Regulation, Developmental ; Heredodegenerative Disorders, Nervous System ; genetics ; Humans ; MicroRNAs ; Neurons ; pathology ; Synapses

BACKGROUND AND OBJECTIVES: Auditory neuropathy is a hearing disorder characterized by the absence or the marked impairment of the auditory brainstem responses with the preservation of the cochlear microphonics (CMs) and otoacoustic emissions. This suggests that outer hair cell (OHC) function is normal but proximal auditory function to OHCs is impaired. It is assumed that the lesion is localized at the level of the inner hair cells (IHCs), auditory nerve fibers, or the synapse between them. This study was aimed to observe the change of hearing threshold and pathology of spiral ganglion cell induced by ouabain application, and present basic data to explain the auditory neuropathy. MATERIALS AND METHOD: Twenty ears of twenty normal hearing cats were used in this study. Cats were treated with 100 microL ouabain (1 mM) applied on the round window. After three days, compound action potential (CAP) and CM were measured and the cochlea was obtained. Pathologic change of spiral ganglion cell was evaluated under light microscope after H&E stain. Normal saline was injected for the control group. RESULTS: In the ouabain group, CAP threshold was increased in all tested frequencies (p<0.001) and the difference of CM threshold was not significant in all frequencies (p>0.05). There was significant difference between CAP and CM threshold shift (p<0.001). In the control group, there was no significant difference in CAP and CM thresholds. Light microscopic findings show that the condensed chromatin and nuclear fragments of spiral ganglion cells of an ear was exposed to ouabain, and outer hair cell and inner hair cell were not damaged. CONCLUSION: This study shows that the CAP threshold was significantly increased but the CM threshold was not changed in the ouabain group. Ouabain induced damage of spiral ganglion cells. This study is not sufficient to explain auditory neuropathy because threshold shift of CAP is not obvious, but it would be helpful to explain that selective damage of spiral ganglion cell would be the mechanism of auditory neuropathy.
Action Potentials ; Animals ; Cats* ; Chromatin ; Cochlea ; Cochlear Nerve ; Ear ; Evoked Potentials, Auditory, Brain Stem ; Hair ; Hearing ; Hearing Disorders ; Ouabain* ; Pathology ; Spiral Ganglion* ; Synapses