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>

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.