Role of curcumin-mediated inhibition of inflammation in alleviating brain ischemia-reperfusion synaptic injury / 公共卫生与预防医学

Objective To investigate the potential effect and mechanism of curcumin in inhibiting synaptic injury in the cortex of rats with cerebral ischemia-reperfusion. Methods Sprague-Dawley rats were divided into sham-operated group, model group, low-dose curcumin (50 mg/kg) group, and high-dose curcumin (100 mg/kg) group. A model of middle cerebral artery occlusion for 2 hours and reperfusion for 24 hours was constructed, and curcumin was administered. Based on the neurological function score, the effects of curcumin on cerebral infarct volume, synaptic ultrastructure changes, inflammatory cell infiltration, and the expression of NLRP3, Caspase-1, Synapsin1, and CAMKⅡ were observed after the end of the animal treatment. Results The neurological function scores were 0, 3.25±0.43, 2.50±0.50, and 1.50±0.50 for the sham-operated group, model group, low-dose curcumin group, and high-dose curcumin group, respectively. The percentage of cerebral infarct volume was 0, (38.89±2.21)%, (33.48±1.77)%, and (23.69±2.19)%, respectively. Compared with the sham operation group, the model group had severe synaptic ultrastructure damage, extensive inflammatory cell infiltration, significantly increased expression of Caspase-1 and NLRP3 (P < 0.5), and significantly decreased expression of Synapsin1 and CAMKⅡ (P < 0.5). Curcumin treatment significantly inhibited synaptic damage, reduced inflammatory cell infiltration, decreased the expression of Caspase-1 and NLRP3 (P < 0.5), and increased the expression of Synapsin1 and CAMKII (P < 0.5), when compared with the model group. Conclusion Ischemia-reperfusion-mediated synaptic injury in rat brain triggers an inflammatory response in cortical nerve cells, and curcumin alleviates synaptic damage and reduces brain injury by inhibiting inflammatory factor levels.

Effects of ephedrine on the expression levels of BDNF, PSD95 and synapsin1 in PC12 cells / 药学实践杂志

Objective To investigate the effects of ephedrine on the expression levels of brain-derived neurotropic factor (BDNF) and postsynaptic density protein 95 (PSD95) and synapsin1 in PC12 cells, and to explore the mechanism of ephedrine cytotoxicity on PC12. Methods After PC12 cells were treated with different concentration of ephedrine, the cell survival rate was measured by the methylthiazolyldiphenyl-tetrazolium bromide (MTT) assay. The morphology changes of PC12 cells were observed by an inverted microscope. Western blot was used to detect the protein expression levels of BDNF, PSD95 and synapsin1 in PC12 cells. Results Ephedrine decreased the viability of PC12 cell in a concentration-dependent manner,with an IC25 and IC50 of 0.536 mmol and 2.8 mmol, respectively, for PC12 cell death. As ephedrine concentration increased, PC12 cells became smaller in size, with blurred boundary blurred, reduced synapses and shorter axon lengths. The expression levels of BDNF and PSD95 increased significantly. Meanwhile the expression level of synapsin1 decreased. Conclusion The mechanism of ephedrine cytotoxicity on PC12 may be related to the expression levels of BDNF, PSD95 and synapsin1.

Comparison of Electroacupuncture at Jiaji (EX-B2) Points and Stomach Meridian Foot-Yang Ming Points on Recovery of Lower Limb Nerve Function and Synapsin I Expression in Spinal Cord Injury Rats / 中国康复理论与实践

Objective:To investigate the effect of electroacupuncture at Jiaji (EX-B2) points and Stomach Meridian Foot-Yang Ming points on the neurological function and the expression of local Synapsin I in rats after spinal cord injury, and to explore its molecular mechanism. Methods:A total of 60 Sprague-Dawley rats were established spinal cord injury model and they were randomly divided into normal control group, Jiaji group and Yang Ming group, with 20 rats in each group. On the third day after operation, Jiaji group and Yang Ming group were treated with electroacupuncture while the normal control group was not. Their neurological function was assessed with BBB every day. Four rats in each group were sacrificed at the end of the 1st, 2nd, 3rd, 4th and 5th week during the intervention period. HE staining was used to observe the morphology of spinal cord. Immumohistochemical staining was used to detect the expression of Synapsin I protein. Reverse transcription real-time quantitative polymerase chain reaction (RT-qPCR) and Western blotting was used to detect the content of of Synapsin I mRNA and protein. Results:The BBB scores were higher in Jiaji group and Yang Ming group than in the normal control group at all the time points (P < 0.05), and were higher in Yang Ming group than in Jiaji group from one to three weeks (P < 0.05). The immunohistochemical scores of Synapsin I protein were higher in Jiaji group than in the normal control group in the first week (P < 0.05), and were higher in Yang Ming group than in the normal control group from one to four weeks (P < 0.05). The immunohistochemical scores of Synapsin I protein were higher in Yang Ming group than in Jiaji group from three to four weeks (P < 0.05). The expression of Synapsin I mRNA and protein first increased and then decreased in the normal control group; which was higher in Jiaji group than in the normal control group in the first week (P < 0.05) and was higher in Yang Ming group than in the normal control group from one to four weeks (P < 0.05). The Synapsin I mRNA expression in the third week and the Synapsin I protein expression from two to three weeks was higher in Yang Ming group than in Jiaji group (P < 0.05). Conclusion:Electroacupuncture at both Jiaji points and Stomach Meridian Foot-Yang Ming points promote the recovery of nerve function in rats with spinal cord injury. It may be related to the elevated level of Synapsin I in the damaged parts of the spinal cord.

The Role of Synapsins in Neurological Disorders / 神经科学通报·英文版

Synapsins serve as flagships among the presynaptic proteins due to their abundance on synaptic vesicles and contribution to synaptic communication. Several studies have emphasized the importance of this multi-gene family of neuron-specific phosphoproteins in maintaining brain physiology. In the recent times, increasing evidence has established the relevance of alterations in synapsins as a major determinant in many neurological disorders. Here, we give a comprehensive description of the diverse roles of the synapsin family and the underlying molecular mechanisms that contribute to several neurological disorders. These physiologically important roles of synapsins associated with neurological disorders are just beginning to be understood. A detailed understanding of the diversified expression of synapsins may serve to strategize novel therapeutic approaches for these debilitating neurological disorders.

Acrylamide-induced Subacute Neurotoxic Effects on the Cerebral Cortex and Cerebellum at the Synapse Level in Rats / 生物医学与环境科学（英文）

<p><b>OBJECTIVE</b>To investigate acrylamide (ACR)-induced subacute neurotoxic effects on the central nervous system (CNS) at the synapse level in rats.</p><p><b>METHODS</b>Thirty-six Sprague Dawley (SD) rats were randomized into three groups, (1) a 30 mg/kg ACR-treated group, (2) a 50 mg/kg ACR-treated group, and (3) a normal saline (NS)-treated control group. Body weight and neurological changes were recorded each day. At the end of the test, cerebral cortex and cerebellum tissues were harvested and viewed using light and electron microscopy. Additionally, the expression of Synapsin I and P-Synapsin I in the cerebral cortex and cerebellum were investigated.</p><p><b>RESULTS</b>The 50 mg/kg ACR-treated rats showed a significant reduction in body weight compared with untreated individuals (P < 0.05). Rats exposed to ACR showed a significant increase in gait scores compared with the NS control group (P < 0.05). Histological examination indicated neuronal structural damage in the 50 mg/kg ACR treatment group. The active zone distance (AZD) and the nearest neighbor distance (NND) of synaptic vesicles in the cerebral cortex and cerebellum were increased in both the 30 mg/kg and 50 mg/kg ACR treatment groups. The ratio of the distribution of synaptic vesicles in the readily releasable pool (RRP) was decreased. Furthermore, the expression levels of Synapsin I and P-Synapsin I in the cerebral cortex and cerebellum were decreased in both the 30 mg/kg and 50 mg/kg ACR treatment groups.</p><p><b>CONCLUSION</b>Subacute ACR exposure contributes to neuropathy in the rat CNS. Functional damage of synaptic proteins and vesicles may be a mechanism of ACR neurotoxicity.</p>

Effect of histone lysine methtyltransferase G9a in sevoflurane-induced long-term cognitive impairments in the developing brain of neonatal rats / 临床麻醉学杂志

Objective To investigate the role of histone lysine methyltransferase G9a in sevoflurane-induced cognitive impairment in the developing brain of neonatal rats.Methods Thirty-six 5-day-old male SD rats were randomly divided into 3 groups (n =12):control group,sevoflurane group and Bix01294 (the inhibitor of histone lysine methyltransferase G9a)group.The rats in the sevoflurane group and the Bix01294 group received 3% sevoflurane anesthesia for 2 hours once a day at postnatal 5-7 days (P5-P7 ).The rats in the Bix01294 group received Bix01294 (10 mg/kg)subcu-taneously at 1 5 min before anesthesia,and the rats in the control group and sevoflurane group received normal saline for injection (0.1 ml)at the same time.The open-field test and fear condition-ing test were performed at P3 5 and P3 9-P41 ,respectively.The tissues of hippocampus were collected at P42 to measure the levels of G9a,histone H3 lysine 9 dimethylation (H3K9me 2 )and synapsin 1. Results Compared with the control group,the percentage of freezing time of sevoflurane group was significantly decreased in the contextual fear condition test,while the levels of G9a and H3K9me 2 were significantly increased and the level of synapsin 1 was significantly decreased (P <0.01).How-ever,the percentage of freezing time of Bix01294 group was significantly increased,while the levels of G9a and H3K9me 2 were significantly decreased and the level of synapsin 1 was significantly in-creased compared with the sevoflurane group (P <0.05).There was no difference in the total distance and residence time in the central grid in the open-field test,and the percentage of freezing time in the cued fear condition test among the three groups.Conclusion Histone lysine methyltransferase G9a is involved in the sevoflurane-induced long-term cognitive impairment in developing brain of neonatal rats,which may be associated with the increase of H3K9me 2 and the down-regulation of synapsin 1 in the hippocampus.

Effects of mild hypothermia on cognitive function and synapsin iexpression , synaptic ultrastructure of hippocampus in epileptic rats induced by global cerebral ischemia / 实用医学杂志

Objective To study the effects of mild hypothermia on cognitive function , synapsinⅠexpression and synaptic ultrastructure of hippocampus in epileptic rats induced by global cerebral ischemia. Methods Forty-eight male SD rats were randomly divided into control (NC) group, sham-operated (Sham) group, normothermic epilepsy (NT) group and mild hypothermic epilepsy (HT) group. The model of postischemic audio-genetic seizure was established by chest compression. Hypothermia intervention was given to HT group. Immunocytochemistry was conducted to detect the expressions of synapsin I in hippocampus at days 1 , 3, 14. the synaptic ultrastructure and cognitive function were respectively observed by electron microscope and Morris water maze. Results Compared with NC and Sham group, the expression of synapsinI in NT group was decreased, the escape latency was prolonged and across platform number decreased (P < 0.05). The synapses were decreased in number, and mitochondria was viewed swelling, synaptic membranes unclear, myelin fractured. Compared with NT group, the expression of synapsinⅠin HT group had no obvious change in 24 h but was significantly increased in days 3 and 14 (P < 0.01); The escape latency was decreased and the number of cross platform increased (P < 0.01); Synaptic structure was clear, with interface growing and postsynaptic density thickened. Conclusion Mild hypothermia may improve the cognitive function of the epileptic rats induced by global cerebral ischemia by upregulating the expression of synapsinⅠand alleviating the damage of synaptic structure.

Expression of synapsin in visual cortex of developing mice / 中华实验眼科杂志

Background The treatment timing and method of amblyopia rely on the plasticity of visual system.Synapsin is a family of presynaptic terminal specific protein.Its role in visual developmental plasticity is below understood.Objective To investigate the dynamic expressions of synapsin (T-synapsin),and phosphorylation of synapsin (p-synapsin Ⅰ a/b) in visual cortex of normal mice and further explore the role of synapsin in plasticity of visual system.Methods Forty-two clean neonatal C57BL/6 mice were collected.The mice were sacrificed at postnatal 7,14,21,28,35,42,60 days respectively to obtain the tissue samples of visual cortex.Expression levels of T-synapsin and p-synapsin in the visual cortex following the ageing were quantitatively detected using Western blot assay.Results The expression of synapsin in normal mice showed a dynamic increase with the ageing.The T-synapsin Ⅰ a/b/β-actin value in visual cortex was (21.32 ± 3.27) ％,(56.27 ± 10.18) ％,(77.05 ± 10.05) ％,(83.75±10.52) ％,(94.69±11.46)％,(98.75±5.86) ％ of adults mice (postnatal 60 days,P60) in the mice of postnatal 7,14,21,28,35,42 days,respectively,showing a significant difference among them (F =69.538,P ＜ 0.001).Compared with the adult mice,the T-synapsin Ⅰ a/b/β-actin value in the mice of P7,P14,P21,P28 was significantly lower (all at P＜0.05),but no significant difference was found between P35 and P60,P42 and P60 (P =0.280,0.798).The development trend of different synapsin subtypes,such as T-synapsin Ⅰ a/b,T-synapsin Ⅱ a,T-synapsin Ⅱ b and T-synapsin Ⅲ a,was not quite the same during the ageing.The expression of T-synapsin Ⅱ a and Ⅲ a increasing more slowly with development,and kept increasing until P60.Significant differences were found among various age of mice in T-synapsin Ⅱ a,Ⅱ b,Ⅲa respectively(F =42.492 55.595,39.172,all at P＜0.001).The p-synapsin Ⅰ a/b level in the visual cortex elevated with the ageing of the mice,and that peaked in P21 mice,which was (2.86±0.17) times more than that in adult mice.After that,the expression level of p-synapsin Ⅰ a/b dropped rapidly.A significant difference was found in the p-synapsin Ⅰ a/b expression among different ages of mice (F =22.620,P ＜ 0.001).Conclusions Synapsin level in visual cortex presents a developmental change which correlated with the onset and decline of the critical period.Synapsin is probably involved in the regulation of neural plasticity in visual cortex in critical period.

Association of CHRNA4 and SYN2 gene polymorphism with febrile seizure in the Han Chinese children / 中华实用儿科临床杂志

Objective To explore whether single nucleotide polymorphism(SNP) of nicotinic acetylcholine receptor subunit α-4(CHRNA4) or synapsin Ⅱ (SYN2) gene can be used as markers of susceptibility to simple febrile seizure(FS) in the Han children of North China.Methods The CHRNA4 gene rs1044396 and SYN2 gene rs3773364 were genotyped by adopting SNaPshot SNP technique in 141 simple FS children and 130 healthy normal controls.The genotype and allele gene frequency in the 2 groups were compared.Results There were no significant differences in the genotype and allele gene in CHRNA4 gene rs1044396 and SYN2 gene rs3773364 between FS children and healthy controls(all P ＞ 0.05) ; As compared with the FS's clinical data of A/A,A/G,G/G genotypes of the CHRNA4 gene rs1044396 polymorphism and C/C,C/T,T/T genotypes of SYN2 gene rs3773364 polymorphism,there was statistically significant difference in age of first onset in rs 1044396 polymorphism (x2 =17.206,P ＜ 0.001),and there were statistically significant differences in ages and temperature of first onset and gender(x2 =21.458,8.717,10.424,all P ＜0.05) in rs3773364.Conclusions There is no association of CHRNA4 gene rs1044396 polymorphism or SYN2 gene rs3773364 polymorphism with the incidence of simple FS in the Han children of North China,but they may be associated with the age and temperature of first onset.

Synapsin-1 and tau reciprocal O-GlcNAcylation and phosphorylation sites in mouse brain synaptosomes

O-linked N-acetylglucosamine (O-GlcNAc) represents a key regulatory post-translational modification (PTM) that is reversible and often reciprocal with phosphorylation of serine and threonine at the same or nearby residues. Although recent technical advances in O-GlcNAc site-mapping methods combined with mass spectrometry (MS) techniques have facilitated study of the fundamental roles of O-GlcNAcylation in cellular processes, an efficient technique for examining the dynamic, reciprocal relationships between O-GlcNAcylation and phosphorylation is needed to provide greater insights into the regulatory functions of O-GlcNAcylation. Here, we describe a strategy for selectively identifying both O-GlcNAc- and phospho-modified sites. This strategy involves metal affinity separation of O-GlcNAcylated and phosphorylated peptides, beta-elimination of O-GlcNAcyl or phosphoryl functional groups from the separated peptides followed by dithiothreitol (DTT) conjugation (BEMAD), affinity purification of DTT-conjugated peptides using thiol affinity chromatography, and identification of formerly O-GlcNAcylated or phosphorylated peptides by MS. The combined metal affinity separation and BEMAD approach allows selective enrichment of O-GlcNAcylated peptides over phosphorylated counterparts. Using this approach with mouse brain synaptosomes, we identified the serine residue at 605 of the synapsin-1 peptide, 603QASQAGPGPR612, and the serine residue at 692 of the tau peptide, 688SPVVSGDTSPR698, which were found to be potential reciprocal O-GlcNAcylation and phosphorylation sites. These results demonstrate that our strategy enables mapping of the reciprocal site occupancy of O-GlcNAcylation and phosphorylation of proteins, which permits the assessment of cross-talk between these two PTMs and their regulatory roles.

Effects of Alpinia oxyphylla fructus on learning-memory and expression of related signal proteins in hippocampus of brain aging mice / 中华行为医学与脑科学杂志

Objective To investigate the effects and mechanisms of Alpinia oxyphylla fructus (AOF) on learning and memory in D-galactose induced brain aging mice. Methods The brain aging model was induced by s. c D-galactose. Learning-memory ability was tested by passive avoidance test and Morris water maze test, and the expression of synapsin ( Syn), mitogen-activated protein kinase (MAPK) and protein kinase ( PKC ) in hippocampus were examined by Western blot. Results ① Passive avoidance test:the latency in brain aging group( ( 119.80 ±101.80)s) significantly decreased,and the number of errors (4.4 ± 1.3 ) significantly increased compared with the control group( latency: (279.30 ± 31.64) s; number of errors: ( 1. 8 ±0.9), P＜0. 01 ) ). The latency in low dose, middle dose and high dose AOF group( ( 170.25 ± 68.31 ) s, (226.31 ± 73.25 ) s, (263.20 ± 70.55 ) s) significantly increased, and the number of errors in middle dose and high dose AOF group ( ( 2.8 ± 1.2 ), ( 2.3 ±0. 9 ) ) significantly decreased compared with brain aging group (P ＜ 0. 05, P ＜ 0. 0 1 ). ② Morris water maze test:the escape latency in brain aging group was significantly longer, and the time spent in the original quadrant that previously contained the platform was significantly shorter compared with the control group (P＜0. 01 ). The escape latency in 3 AOF groups was significantly shorter (P＜ 0. 05 ), and the time spent in the original quadrant that previously contained the platform in middle and high dose AOF groups was significantly longer compared with brain aging group (P＜0. 05, P＜0. 01 ). ③ Western blot test:the expression of Syn,MAPK and PKC in hippocampus of brain aging group was significantly weakened than that of the control group. In contrast, the expression of Syn,MAPK, PKC were significantly enhanced in all AOF groups. Conclusion AOF could significantly improve the ability of learning and memory in brain aging mice. Its effects might be related to the increase of the expression of Syn, MAPK and PKC in hippocampus.

Expression of synapsin and dopamine transporter mRNA in hippocampus of chronic stress depression model rats / 中华行为医学与脑科学杂志

Objective To study the mechanism of depression by explore the expressional differences of synapsin and dopamine transporter(DAT) mRNA of hippocampus in depression model rats. Methods Depression model were replicated by chronic stress. 20 rats were randomly divided into normal control group(n=10) and de-pression model group(n=10). Synapsin and DAT mRNA expressions in hippocampns were detected with RT-PCR technique. Result The values of synapsin and DAT mRNA in hippocampus of normal control group were 0.84±0.08 and 1.24±0.08, respectively, and 1.24±0.12 and 1.85±0.09 of model group, their t values were 8.87 and 16.50 (P<0.01). Conclusion The expressions of synapsin and DAT mRNA in hippecampus of depression model rats were increased significantly.

Type 2 Iodothyronine Deiodinase Activity and Expressions of MBP and Synapsin I in Brain of Young Rats with Iodine Deficiency and Excess / 环境与健康杂志

Objective To study the activity of type 2 Iodothyronine deiodinase(D2)and the expressions of myelin basic protein(MBP)and synapsinⅠin the brain tissue of young rats fed on a diet with different levels of iodine.Methods Wistar rats were fed on a diet with different doses of KIO_3 for 3 months and then mated randomly.The serum TH and the brain D2 activity were measured in 28 days old pups.The protein expressions of MBP and SynapsinⅠin their brains were determined by immunohistochemistry staining.Results Compared with normal iodine group(NI),the serum TH levels of low iodine group(LI) were lower,while those of iodine excess groups were gradually decreased with their increase of iodine intake,especially in 100-fold high iodine group(100 HI),TT_4 and FT_4 were significantly decreased(P0.05).The immunohistochemistry staining showed weakly positive reactivity of MBP in corpus callosum and stronger of synapsin I in hippocampus CA3 in LI group compared with NI. The similar alterations were also found in all iodine excess groups with their increase of iodine intake.But MBP reactivity was stronger in 100 HI rats than the LI ones.Conclusion Iodine deficiency and iodine excess can cause hypothyroidism in degrees in the young rats,more severe hypothyroid and retarded myelin sheath and synapses can be caused in iodine deficiency compared with iodine excess.

Jiuqiang Naoliqing enhancing the expression of CGRP and Synapsin Ⅰ in brain of spontaneous hypertension rats / 中国康复理论与实践

@#ObjectiveTo study the influence of Jiuqiang Naoliqing (JNQ) on the expression of calcitonin gene related peptide(CGRP)and Synapsin Ⅰ in brain of the spontaneous hypertension rats (SHR). MethodsThe rats were randomly divided into 4 groups: Wistar group, SHR group, lower dose of JNQ treated SHR group and higher dose of JNQ treated SHR group. The expression of CGRP and Synapsin Ⅰ in the dentate gyrus, CA1 subfield of hippocampus and cortex were determined by immunohistochemistry after treatment for 3 weeks. ResultsCompared with the Wistar group, the expression of CGRP and Synapsin Ⅰ in the dentate gyrus, CA1 subfield of hippocampus and cortex of SHR group significantly decreased. The treatment with lower dose of JNQ significantly enhanced the expression of CGRP in cortex(P<0.05 vs SHR).The treatment with higher dose of JNQ significantly enhanced not only the expression of CGRP in the dentate gyrus, CA1 subfield of hippocampus and cortex, but also that of Synapsin Ⅰ in the CA1 subfield of hippocampus selectively in comparison with SHR group. ConclusionJNQ may improve the micro circulation in brain by up regulating the expression of CGRP and enhance the modulating function of central nervous system by up regulating the expression of Synapsin Ⅰ in spontaneous hypertension rats.

Increase of Synapsin I, Phosphosynapsin (ser-9), and GAP-43 in the Rat Hippocampus after Middle Cerebral Artery Occlusion

The loss of neurons and synaptic contacts following cerebral ischemia may lead to a synaptic plastic modification, which may contribute to the functional recovery after a brain lesion. Using synapsin I and GAP-43 as markers, we investigated the neuronal cell death and the synaptic plastic modification in the rat hippocampus of a middle cerebral artery occlusion (MCAO) model. Cresyl violet staining revealed that neuronal cell damage occurred after 2 h of MCAO, which progressed during reperfusion for 2 weeks. The immunoreactivity of synapsin I and GAP-43 was increased in the stratum lucidum in the CA3 subfield as well as in the inner and outer molecular layers of dentate gyrus in the hippocampus at reperfusion for 2 weeks. The immunoreactivity of phosphosynapsin was increased in the stratum lucidum in the CA3 subfield during reperfusion for 1 week. Our data suggest that the increase in the synapsin I and GAP-43 immunoreactivity probably mediates either the functional adaptation of the neurons through reactive synaptogenesis from the pre-existing presynaptic nerve terminals or the structural remodeling of their axonal connections in the areas with ischemic loss of target cells. Furthermore, phosphosynapsin may play some role in the synaptic plastic adaptations before or during reactive synaptogenesis after the MCAO.

Translocational changes of localization of synapsin in axonal sprouts of regenerating rat sciatic nerves after ligation crush injury

Time-dependent translocational changes of Synapsin I (SyI), a synaptic vesicle-associated phosphoprotein and its involvement in the axonal transport were investigated in the regenerating axonal sprouts. A weak SyI immunoreactivity (IR) was found in the axoplasm of normal axons. Rat sciatic nerves were crush-injured by ligating with 1-0 silk thread at the mid-thigh level and released from the ligation 24 h later. At various times after release, immunocytochemistry was performed. SyI was translocated from the proximal to the distal site of ligation and also involved in the sprouting of regenerating axons. The distribution patterns of SyI IR were changed in the crush-injured nerves. SyI immunoreactive thin processes were strongly appeared in the proximal region from 1 h after release. After 3 h, a very strong IR was expressed. The intense SyI immunoreactive thin processes were elongated distally and were changed the distribution pattern by time-lapse. After 12 h, strong immunoreactive processes were extended to the ligation crush site. At 1 day, a very intense IR was expressed. At 2 days, immunoreactive thin processes extended into the distal region over the ligation crush site and strong IR was observed after 3 days. SyI was accumulated in the proximal region at the early phases after release. These results suggest that SyI may be related to the translocation of vesicles to the elongated membranes by a fast axonal transport in the regenerating sprouts.

Effect of synapsin-Ⅰ antisense oligonucleotide on neural differentiation of embryonic stem cells in vitro / 中华神经科杂志

Objective To investigate the role of synapsin-I in the differentiation of the embryonic stem cells (ESC) into the neuron,and to seek a controllable point for the ESC neural differentiation in vitro.Methods Neural differentiation of ESC was induced with the "five step approach",synapsin-I antisense oligonucleotides (AS ONs) was employed to inhibit the synapsin-I expression at different stages. At different time points,morphology,differentiation efficiency and neural specific markers were compared among the normal group and the transfected groups.A tumor cell line called PC12 cell was compared with the ESC at the same time.Results After the synapsin-I AS ONs were used in ESC differentiation, considerable decreases of neurite growth rate and neural precursor cells (nestin (+)) percentage were observed at Stage 3(68.5%?4.2% vs 76.2%?5.1% and 75.8%?4.9%,P

Evaluation of end-to-side neurorrhaphy / 实用口腔医学杂志

Objective:To evaluate functional recovery of nerve and muscle after end-to-side neurorrhaphy.Methods:10 SD rats were randomly and evenly devided into group A and group B.Right common peroneal nerve was amputated in all the rats.Then the distal stump was sutured to the ipsilateral tibial nerve by the end-to-side way through a epineurial window in group A. The right common peroneal nerve was severed in group B as denervated control.After 1.5 months all the rats were subjected to walking track analysis,histological and ultrastructure observation.Results:In group A peroneal nerve index (PFI) achieved -41.634,density of collateral axons 51.437?12.041/1 000 ?m 2,synapsin (SYP) 439?120.5.In group B PFI was -100,SYP 0. In normal control PFI was 0, density of collateral axons 18.847?1.078/1 000 ?m 2,SYP 842?84.7.Conclusion:End-to-side neurorrhaphy may induce nerve sprout plenty of collateral axons.The axons can reach target muscle to reconstruct functional neuromuscular junction,and recover the function of the muscle in some degree.

Changes of synapsin Ⅰ expression and synaptic ultrastructure in hippocampus of the rat models of epilepsy / 临床神经病学杂志

Objective To illuminate relationships between epilepsy and functional and morphologic plasticity of synapse through investigating temporal-spatial expression of syanpsinⅠand the alteration of synaptic ultrastructure in hippocampus after seizure. Methods The models of epilepsy were established by injection of pilocarpine and lithium. Electromicroscope and the software of image manipulation were applied to observe the alteration of synaptic ultrastructure in hippocampus during acute phase, resting phase and chronic phase. The expressions of synapsinⅠ were determined by immunohistochemistry. Results The expression of synapsinⅠin every subfield of hippocampus decreased at 3 h after induction of seizure, reached the peak at 6 h and 12 h, which was significantly different from the control ( P

Effect of (-)clausenamide on potentiating synaptic transmission in dentate gyrus:Role of synapsin Ⅰ / 中国药理学通报

Aim To study the effect of synapsinⅠon synaptic transmission in rat dentate gyrus induced by(-) clausenamide.Methods The basal synaptic transmission experiment was conducted through electrophysiological recordings.The effect of(-) clausenamide on synapsinⅠ phosphorylation was measured by western blot and confocal microscopy.Results(-)Clausenamide increased the population spike(PS) of hippocampal dentate gyrus.The phosphorylation of synapsinⅠ was increased both in cortex and hippocampus,the maximum effect was observed at 5 min in hippocampus and at 15 min in cortex.Furthermore,(-)clausenamide promoted the phosphorylation of synapsinⅠat a dose-denpendent manner in PC12 cells.The phosphorylation of synapsinⅠ in PC12 cells and synaptosomes incubated with(-)clausenamide was increased and reached maximum at 1~2 min.However,H89,PKA inhibitor,blocked the effect of(-)clausenamide on synapsinⅠ phosphorylation.Conclusion(-)Clausenamide activated synapsinⅠ via PKA signal pathway,which may contribute to the effect of(-)clausenamide on potentiating basal synaptic transmission.