Hair Cells, Auditory, Inner ; cytology ; Synapses ; physiology ; ultrastructure

AIMTo observe the effect of fimbria-fornix (FF) transection on rat's hippocampal synaptic configuration.

METHODSAnimal models were produced by transecting rat's bilateral fimbria-fornix (FF). Y-type maze test were carried out respectively before and after the models were built, and emphasis was laid on the quantitative analyses of the parameters of synapses in the hippocampal CA3 areas.

RESULTSThe thickness of postsynaptic density material, the curvature of synaptic interface and the occurrence of perforated synapses decreased, while the width of synaptic cleft increased.

CONCLUSIONFimbria-fornix transection resulted in evident changes of the synaptic configuration in the hippocampal CA3 areas and we presume that the normal Ach level in the hippocampus plays a key role in maintaining the normal synaptic interface ultrastructure of the hippocampus CA3 area.

Animals ; CA3 Region, Hippocampal ; metabolism ; ultrastructure ; Fornix, Brain ; surgery ; Male ; Neurons ; Rats ; Rats, Sprague-Dawley ; Synapses ; ultrastructure

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

By using stereological morphometric techniques, we examined the ultrastructure of synapses in lamine II of the spinal dorsal horn of Sprague Dawley rats 30 min, 3 h and 5 h after long-term potentiation (LTP) induction. We found that the numerical density per unit volume (Nv) of total synapses, the thickness of the postsynaptic density (PSD), width of the synaptic cleft increased significantly after the establishment of LTP. (1) Thirty minutes after the formation of LTP, the thickness of the PSD increased from 0.029 +/-0.0064 microm (control) to 0.036 +/-0.009 microm (P<0.05) and the width of the synaptic cleft increased from 0.0181+/-0.0024 microm (control) to 0.0197+/-0.0029 microm (P< 0.05); the number of synaptic vesicles decreased from 0.122 +/-0.011/microm(2) to 0.085 +/-0.010/microm(2) (P<0.05); (2) 3 h after the formation of LTP, the thickness of PSD and the width of the synaptic cleft had no difference compared with those 30 min after LTP. The number of synaptic vesicles increased from 0.122 +/-0.011/microm(2) to 0.138 +/-0.015/microm(2); the curvature of the synaptic interface increased from 1.153+/-0.195 to 1.386 +/-0.311 (P<0.05, compared with control). Nv of negative synapses increased from 0.0187 +/-0.0056 to 0.0543 +/-0.0152 (P<0.05, compared with control), Nv of perforated synapses also increased from 0.0135 +/-0.0053 to 0.0215 +/-0.0076 (P<0.05, compared with control). These data suggest that the increase in thickness of PSD might be the major morphological change during the induction of LTP, while the increase in curvature of the synaptic interface, and the number of perforated synapses might be responsible for the maintenance of the spinal LTP.
Animals ; Long-Term Potentiation ; physiology ; Male ; Posterior Horn Cells ; physiology ; ultrastructure ; Rats ; Spinal Cord ; anatomy & histology ; physiology ; Synapses ; ultrastructure ; Synaptic Transmission ; Synaptic Vesicles ; ultrastructure

The regulation of astroglia on synaptic plasticity in the CA1 region of rat hippocampus was examined. Rats were divided into three groups: the newly born (< 24 h), the juvenile (28-30 days) and the adult groups (90 - 100 days), with each group having 20 animals. The CA1 region of rat hippocampus was immunohistochemically and electron-microscopically examined, respectively, for the growth of astroglia and the ultrastructure of synapses. The high performance liquid chromatography was employed to determine the cholesterol content of rat hippocampus. In the newly-born rats, a large number of neurons were noted in the hippocampal CA1 region of the newly-born rats, and few astroglia and no synaptic structure were observed. In the juvenile group, a few astroglias and some immature synapses were found, which were less than those in adult rats (P < 0.01). The cholesterol content was 2.92 +/- 0.03 mg/g, 11.20 +/- 3.41 mg/g and 12.91 +/- 1.25 mg/g for newly born, the juvenile and the adult groups, respectively, with the differences among them being statistically significant (P < 0.01). Our study suggests that the astrocytes may play an important role in the synaptic formation and functional maturity of hippocampal neurons, which may be related to the secretion of cholesterol from astrocytes.
Age Factors ; Animals, Newborn ; Astrocytes/cytology ; Astrocytes/metabolism ; Astrocytes/*physiology ; CA1 Region, Hippocampal/*physiology ; CA1 Region, Hippocampal/*ultrastructure ; Cell Communication/physiology ; Cholesterol/metabolism ; Neuronal Plasticity/*physiology ; Random Allocation ; Rats, Wistar ; Synapses/*physiology ; Synapses/ultrastructure

The prenatal ethanol exposure induced the alterations of dendritic spine and synapse in visual cortex and their long-term effect would be investigated in mice from P0 to P30. Pregnant mice were intubated ethanol daily from E5 through the pup's birth to establish mode of prenatal alcohol abuse. The dendritic spines of pyramidal cells in visual cortex of pups were labeled with DiI diolistic assay, and the synaptic ultrastructure was observed under transmission electron microscope. Prenatal alcohol exposure was associated with a significant decrease in the number of dendritic spines of pyramidal neurons in the visual cortex and an increase in their mean length; ultrastructural changes were also observed, with decreased numbers of synaptic vesicles, narrowing of the synaptic cleft and thickening of the postsynaptic density compared to controls. Prenatal alcohol exposure is associated with long-term changes in dendritic spines and synaptic ultrastructure. The changes were dose-dependent with long term effect even at postnatal 30.
Animals ; Dendritic Spines ; ultrastructure ; Ethanol ; toxicity ; Female ; Fetal Alcohol Spectrum Disorders ; etiology ; pathology ; Male ; Mice ; Mice, Inbred C57BL ; Microscopy, Confocal ; Microscopy, Electron, Transmission ; Pregnancy ; Prenatal Exposure Delayed Effects ; pathology ; Pyramidal Cells ; ultrastructure ; Synapses ; ultrastructure ; Visual Cortex ; ultrastructure

Amino Acids ; metabolism ; Animals ; Dose-Response Relationship, Radiation ; Hippocampus ; metabolism ; radiation effects ; Male ; Microwaves ; adverse effects ; Neurons ; radiation effects ; ultrastructure ; Rats ; Rats, Wistar ; Synapses ; radiation effects ; ultrastructure

Synaptic ultrastructural changes after long-lasting long-term potentiation (L-LTP) induced by 2 and 100 Hz tetanus were investigated by electron microscopic and stereological approach in slices of the developing rat visual cortex (postnatal days 15~21). Both 2 and 100 Hz tetanus-induced L-LTP groups showed significant increases in synaptic interface curvature, synaptic numeric density and postsynaptic density thickness, as well as significant decreases in the cleft width, as compared with the control groups. In addition, the volume density of the active zone (AZ) was increased significantly in the 100 Hz tetanus-induced L-LTP group, but not in the 2 Hz group. The mean lateral area of individual AZ in the 100 Hz group was relatively higher than that in the 2 Hz group. These data suggest that newly formed synapses in the 100 Hz tetanus-induced L-LTP group are larger than those in the 2 Hz group and that 100 Hz tetanus might trigger reorganization or synthesis of postsynaptic cytoskeleton.
Animals ; Animals, Newborn ; Electric Stimulation ; methods ; Long-Term Potentiation ; physiology ; Male ; Rats ; Rats, Sprague-Dawley ; Synapses ; ultrastructure ; Synaptic Transmission ; physiology ; Visual Cortex ; physiology ; ultrastructure

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 observe the effect of Kangxin Capsule (KXC) on the expression of nerve growth factor (NGF) as well as the morphology and amount of nerve synapse in the cortical parietal lobe and hippocampus CA, area of vascular dementia ( VD) model rats.

METHODSThe model rats of VD made by photochemical reaction technique were randomly divided into five groups: the model group (MG), the high-dose, middle-dose and low-dose KXC groups (HDG, MDG and LDG), and the Western medicine hydergin control group (WMG). They were treated respectively with distilled water, high, middle and low dosage of KXC suspended liquid, and hydergin for a month. Besides, a blank group consisting of normal (non-model) rats was set up for control (CG). The ultrastructure of nerve synapse in the cortical parietal lobe and hippocampus CA1 area of the rats were observed and its density estimated. The condition of NGF positive neurons in the above-mentioned two regions were also observed by immunohistochemical stain.

RESULTSAll the KXC or hydergin treated groups demonstrated a normal amount of nerve synapse with integral structure in the cortical parietal lobe and hippocampus CA, area, which approached that in the CG and was superior to that in the MG. Also, the NGF positive neuron in all the treated groups was much more than that in MG with significant difference ( P<0.01), approaching to that in the CG.

CONCLUSIONKXC could elevate the expression of NGF in the cortical parietal lobe and hippocampus CA, area, preserve the number and morphology of synapse, thus to protect the function of nerve system from ischemic injury.

Animals ; Capsules ; Dementia, Vascular ; drug therapy ; metabolism ; pathology ; Disease Models, Animal ; Female ; Hippocampus ; chemistry ; Immunohistochemistry ; Male ; Medicine, Chinese Traditional ; Microscopy, Electron ; Nerve Growth Factors ; analysis ; Neurons ; ultrastructure ; Parietal Lobe ; chemistry ; Rats ; Rats, Wistar ; Synapses ; ultrastructure