This study investigated effects of post-training treatment with phaclofen, GABAB receptor antagonist, on the memory of food location and on the expression of Synapsin I in the hippocampus of pigeons. Pigeons were trai...This study investigated effects of post-training treatment with phaclofen, GABAB receptor antagonist, on the memory of food location and on the expression of Synapsin I in the hippocampus of pigeons. Pigeons were trained in food location (7 sessions) and underwent post-training treatment with phaclofen (0.3 mg/kg, i.p.;PHAC), saline (SAL) or non-treated (NTR). Testing for memory persistence occurred 7 days after the last training session (PHACR, SALR and NTRR Groups). Pigeons treated with phaclofen had lower latency and higher correct choice values than saline and non-treated controls (p < 0.05). Analysis of hippocampus tissue indicated that Synapsin I-positive cell counts were higher in pigeons treated with phaclofen than in saline and non-treated controls (p < 0.05). Data indicated enhancement of consolidation and persistence of food location memory, and up-regulation of Synapsin I expression in the hippocampus of pigeons, which were related with post-training blockade of GABAB receptors.展开更多
To define whether oxidative stress and aging induce abnormal dissociation of neurotransmitter-enclosing synaptic vesicles in rat brain nerve terminals, we assessed the activation of Ca+/calmodulin dependent protein ki...To define whether oxidative stress and aging induce abnormal dissociation of neurotransmitter-enclosing synaptic vesicles in rat brain nerve terminals, we assessed the activation of Ca+/calmodulin dependent protein kinase II (CAM kinase II) and changes in the levels of synapsin I, which is a synaptic vesicle-associated protein involved in the modulation of neurotransmitter release. Assessment of young rats subjected to hyperoxia-induced oxidative stress and normal aged rats revealed that synaptic CAM kinase II in the rat brain was markedly activated through oxidative stress and aging. In accordance with the activation of CAM kinase II, the levels of phosphorylated synapsin I increased significantly in nerve terminals. Furthermore, it was found that vitamin E prevents these oxidative stress-induced abnormal processes in rat nerve terminals. These results suggest that oxidative stress and aging facilitate the mobilization of neurotransmitter-enclosing synaptic vesicles from the reserve pool in the nerve terminal, thereby inducing abnormal accumulation of synaptic vesicles in the synapse, and that vitamin E inhibits this process in the brain through its antioxidative action.展开更多
Objective: The aim of this study was to research the relationship between Attention Deficit Hyperactivity Disorder (ADHD) and the synapsin III -196G>A and -631C>G polymorphisms and study their impact on neurocog...Objective: The aim of this study was to research the relationship between Attention Deficit Hyperactivity Disorder (ADHD) and the synapsin III -196G>A and -631C>G polymorphisms and study their impact on neurocognition and behavior in Turkish children and adolescents. Methods: A total of 201 ADHD-diagnosed children and 100 control subjects aged between 8 and 15 years were recruited, and genetic material was obtained from saliva. In the diagnostic assessments, the KSADS- PL semi-structured interview was applied. Children with any comorbid psychiatric diagnosis (with the exclusion of oppositional defiant disorder (ODD)), medical conditions, prior psychotropic drug use history or IQ score below 80 were excluded. For the behavioral and ADHD symptom assessments, the Turgay DSM-IV Disruptive Behaviors Rating Scale, Teacher Report Form (TRF) and Child Behavior Checklist (CBCL) were completed by the parents and teachers. Neurocognitive profiles were evaluated with the CNS-Vital Signs computerized neurocognitive test battery. Results: No significant difference in ADHD prevalence was observed between subjects with the synapsin III gene -196G>A polymorphism and -631C>G polymorphisms. These polymorphisms were also not associated with subtypes of ADHD. We found a relationship between both polymorphisms and Stroop simple reaction time. Conclusion: Synapsin’s effect could be limited during childhood, but synapsin polymorphisms could be associated with Stroop simple reaction time.展开更多
Xuefu Zhuyu decoction has been used for treating traumatic brain injury and improving post-traumatic dysfunction, but its mechanism of action needs further investigation. This study established rat models of traumatic...Xuefu Zhuyu decoction has been used for treating traumatic brain injury and improving post-traumatic dysfunction, but its mechanism of action needs further investigation. This study established rat models of traumatic brain injury by controlled cortical impact. Rat models were intragastrically administered 9 and 18 g/kg Xuefu Zhuyu decoction once a day for 14 or 21 days. Changes in neurological function were assessed by modified neurological severity scores and the Morris water maze. Immunohistochemistry, western blot assay, and reverse-transcription polymerase chain reaction were used to analyze synapsin protein and m RNA expression at the injury site of rats. Our results showed that Xuefu Zhuyu decoction visibly improved neurological function of rats with traumatic brain injury. These changes were accompanied by increased expression of synaptophysin, synapsin Ⅰ, and postsynaptic density protein-95 protein and m RNA in a dose-dependent manner. These findings indicate that Xuefu Zhuyu decoction increases synapsin expression and improves neurological deficits after traumatic brain injury.展开更多
Brain-derived neurotrophic factor (BDNF) promotes synaptic formation and functional maturation by upregulating synapsin expression in cortical and hippocampal neurons. However, it remains controversial whether BDNF af...Brain-derived neurotrophic factor (BDNF) promotes synaptic formation and functional maturation by upregulating synapsin expression in cortical and hippocampal neurons. However, it remains controversial whether BDNF affects synapsin expression in spinal cord anterior horn neurons. Wistar rat spinal cord anterior horn neurons were cultured in serum-supplemented medium containing BDNF, BDNF antibody, and Hank's solution for 3 days, and then synapsin I and synaptophysin protein and mRNA expression was detected. Under serum-supplemented conditions, the number of surviving neurons in the spinal cord anterior horn was similar among BDNF, anti-BDNF, and control groups (P > 0.05). Synapsin I and synaptophysin protein and mRNA expressions were increased in BDNF-treated neurons, but decreased in BDNF antibody-treated neurons (P < 0.01). These results indicated that BDNF significantly promotes synapsin I and synaptophysin expression in in vitro-cultured rat spinal cord anterior horn neurons.展开更多
Synapsin Ⅱ is a member of the neuronal phosphoprotein family. These phosphoproteins are evolutionarily conserved across many organisms and are important in a variety of synaptic functions, including synaptogenesis an...Synapsin Ⅱ is a member of the neuronal phosphoprotein family. These phosphoproteins are evolutionarily conserved across many organisms and are important in a variety of synaptic functions, including synaptogenesis and the regulation of neurotransmitter release. A number of genome-wide scans, meta-analyses, and genetic susceptibility studies have implicated the synapsin II gene(3p25) in the etiology of schizophrenia(SZ) and other psychiatric disorders. Further studies have found a reduction of synapsin II m RNA and protein in the prefrontal cortex in post-mortem samples from schizophrenic patients. Disruptions in the expression of this gene may cause synaptic dysfunction, which can result in neurotransmitter imbalances, likely contributing to the pathogenesis of SZ. SZ is a costly, debilitating psychiatric illness affecting approximately 1.1% of the world's population, amounting to 51 million people today. The disorder is characterized by positive(hallucinations, paranoia), negative(social withdrawal, lack of motivation), and cognitive(memory impairments, attention deficits) symptoms. This review provides a comprehensive summary of the structure, function, and involvement of the synapsin family, specifically synapsin II, in the pathophysiology of SZ and possible target for therapeutic intervention/implications.展开更多
Schizophrenia(SCZ)is the most common serious mental illness with a high disability rate and heavy social and family burdens.At present,there is no clear etiology and pathogenesis of schizophrenia.Studies have shown th...Schizophrenia(SCZ)is the most common serious mental illness with a high disability rate and heavy social and family burdens.At present,there is no clear etiology and pathogenesis of schizophrenia.Studies have shown that the occurrence of schizophrenia may be related to the abnormality of the hypothalamic-pituitary-adrenal(HPA)axis.The LIM-homeobox gene 3(LHXS)and early growth response 1(EGR1)can affect pituitary function.Because the synapsin 2(SYN2)gene polymorphism regulates the activity of LHX3 and EGR1,it may cause the occurrence of schizophrenia.This article will review the possible involvement of SYN2 gene polymorphism in the pathogenesis of schizophrenia via regulating the activity of LHX3 and EGR1,then to afiect the HPA axis.展开更多
Paired associative stimulation has been used in stroke patients as an innovative recovery treatment.However,the mechanisms underlying the therapeutic effectiveness of paired associative stimulation on neurological fun...Paired associative stimulation has been used in stroke patients as an innovative recovery treatment.However,the mechanisms underlying the therapeutic effectiveness of paired associative stimulation on neurological function remain unclear.In this study,rats were randomly divided into middle cerebral occlusion model(MCAO)and paired associated magnetic stimulation(PAMS)groups.The MCAO rat model was produced by middle cerebral artery embolization.The PAMS group received PAMS on days 3 to 20 post MCAO.The MCAO group received sham stimulation,three times every week.Within 18 days after ischemia,rats were subjected to behavioral experiments—the foot-fault test,the balance beam walking test,and the ladder walking test.Balance ability was improved on days 15 and 17,and the footfault rate was less in their affected limb on day 15 in the PAMS group compared with the MCAO group.Western blot assay showed that the expression levels of brain derived neurotrophic factor,glutamate receptor 2/3,postsynaptic density protein 95 and synapsin-1 were significantly increased in the PAMS group compared with the MCAO group in the ipsilateral sensorimotor cortex on day 21.Resting-state functional magnetic resonance imaging revealed that regional brain activities in the sensorimotor cortex were increased in the ipsilateral hemisphere,but decreased in the contralateral hemisphere on day 20.By finite element simulation,the electric field distribution showed a higher intensity,of approximately 0.4 A/m^2,in the ischemic cortex compared with the contralateral cortex in the template.Together,our findings show that PAMS upregulates neuroplasticity-related proteins,increases regional brain activity,and promotes functional recovery in the affected sensorimotor cortex in the rat MCAO model.The experiments were approved by the Institutional Animal Care and Use Committee of Fudan University,China(approval No.201802173 S)on March 3,2018.展开更多
Impaired hippocampal neurogenesis is one of the early pathological features of Alzheimer's disease. Enhancing adult hippocampal neurogenesis has been pursued as a potential therapeutic strategy for Alzheimer's...Impaired hippocampal neurogenesis is one of the early pathological features of Alzheimer's disease. Enhancing adult hippocampal neurogenesis has been pursued as a potential therapeutic strategy for Alzheimer's disease. Recent studies have demonstrated that environmental novelty activates β2-adrenergic signaling and prevents the memory impairment induced by amyloid-β oligomers. Here, we hypothesized that β2-adrenoceptor activation would enhance neurogenesis and ameliorate memory deficits in Alzheimer's disease. To test this hypothesis, we investigated the effects and mechanisms of action of β2-adrenoceptor activation on neurogenesis and memory in amyloid precursor protein/presenilin 1(APP/PS1) mice using the agonist clenbuterol(intraperitoneal injection, 2 mg/kg). We found that β2-adrenoceptor activation enhanced hippocampal neurogenesis, ameliorated memory deficits, and increased dendritic branching and the density of dendritic spines. These effects were associated with the upregulation of postsynaptic density 95, synapsin 1 and synaptophysin in APP/PS1 mice. Furthermore, β2-adrenoceptor activation decreased cerebral amyloid plaques by decreasing APP phosphorylation at Thr668. These findings suggest that β2-adrenoceptor activation enhances neurogenesis and ameliorates memory deficits in APP/PS1 mice.展开更多
Objective To investigate acrylamide(ACR)-induced subacute neurotoxic effects on the central nervous system(CNS) at the synapse level in rats. Methods Thirty-six Sprague Dawley(SD) rats were randomized into three group...Objective To investigate acrylamide(ACR)-induced subacute neurotoxic effects on the central nervous system(CNS) at the synapse level in rats. Methods 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. Results 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. Conclusion Subacute ACR exposure contributes to neuropathy in the rat CNS. Functional damage of synaptic proteins and vesicles may be a mechanism of ACR neurotoxicity.展开更多
文摘This study investigated effects of post-training treatment with phaclofen, GABAB receptor antagonist, on the memory of food location and on the expression of Synapsin I in the hippocampus of pigeons. Pigeons were trained in food location (7 sessions) and underwent post-training treatment with phaclofen (0.3 mg/kg, i.p.;PHAC), saline (SAL) or non-treated (NTR). Testing for memory persistence occurred 7 days after the last training session (PHACR, SALR and NTRR Groups). Pigeons treated with phaclofen had lower latency and higher correct choice values than saline and non-treated controls (p < 0.05). Analysis of hippocampus tissue indicated that Synapsin I-positive cell counts were higher in pigeons treated with phaclofen than in saline and non-treated controls (p < 0.05). Data indicated enhancement of consolidation and persistence of food location memory, and up-regulation of Synapsin I expression in the hippocampus of pigeons, which were related with post-training blockade of GABAB receptors.
文摘To define whether oxidative stress and aging induce abnormal dissociation of neurotransmitter-enclosing synaptic vesicles in rat brain nerve terminals, we assessed the activation of Ca+/calmodulin dependent protein kinase II (CAM kinase II) and changes in the levels of synapsin I, which is a synaptic vesicle-associated protein involved in the modulation of neurotransmitter release. Assessment of young rats subjected to hyperoxia-induced oxidative stress and normal aged rats revealed that synaptic CAM kinase II in the rat brain was markedly activated through oxidative stress and aging. In accordance with the activation of CAM kinase II, the levels of phosphorylated synapsin I increased significantly in nerve terminals. Furthermore, it was found that vitamin E prevents these oxidative stress-induced abnormal processes in rat nerve terminals. These results suggest that oxidative stress and aging facilitate the mobilization of neurotransmitter-enclosing synaptic vesicles from the reserve pool in the nerve terminal, thereby inducing abnormal accumulation of synaptic vesicles in the synapse, and that vitamin E inhibits this process in the brain through its antioxidative action.
文摘Objective: The aim of this study was to research the relationship between Attention Deficit Hyperactivity Disorder (ADHD) and the synapsin III -196G>A and -631C>G polymorphisms and study their impact on neurocognition and behavior in Turkish children and adolescents. Methods: A total of 201 ADHD-diagnosed children and 100 control subjects aged between 8 and 15 years were recruited, and genetic material was obtained from saliva. In the diagnostic assessments, the KSADS- PL semi-structured interview was applied. Children with any comorbid psychiatric diagnosis (with the exclusion of oppositional defiant disorder (ODD)), medical conditions, prior psychotropic drug use history or IQ score below 80 were excluded. For the behavioral and ADHD symptom assessments, the Turgay DSM-IV Disruptive Behaviors Rating Scale, Teacher Report Form (TRF) and Child Behavior Checklist (CBCL) were completed by the parents and teachers. Neurocognitive profiles were evaluated with the CNS-Vital Signs computerized neurocognitive test battery. Results: No significant difference in ADHD prevalence was observed between subjects with the synapsin III gene -196G>A polymorphism and -631C>G polymorphisms. These polymorphisms were also not associated with subtypes of ADHD. We found a relationship between both polymorphisms and Stroop simple reaction time. Conclusion: Synapsin’s effect could be limited during childhood, but synapsin polymorphisms could be associated with Stroop simple reaction time.
基金supported by the National Natural Science Foundation of China,No.81673719,81173175 and 81303074a grant from China Postdoctoral Science Foundation,No.2016M600639 and 2017T100614
文摘Xuefu Zhuyu decoction has been used for treating traumatic brain injury and improving post-traumatic dysfunction, but its mechanism of action needs further investigation. This study established rat models of traumatic brain injury by controlled cortical impact. Rat models were intragastrically administered 9 and 18 g/kg Xuefu Zhuyu decoction once a day for 14 or 21 days. Changes in neurological function were assessed by modified neurological severity scores and the Morris water maze. Immunohistochemistry, western blot assay, and reverse-transcription polymerase chain reaction were used to analyze synapsin protein and m RNA expression at the injury site of rats. Our results showed that Xuefu Zhuyu decoction visibly improved neurological function of rats with traumatic brain injury. These changes were accompanied by increased expression of synaptophysin, synapsin Ⅰ, and postsynaptic density protein-95 protein and m RNA in a dose-dependent manner. These findings indicate that Xuefu Zhuyu decoction increases synapsin expression and improves neurological deficits after traumatic brain injury.
文摘Brain-derived neurotrophic factor (BDNF) promotes synaptic formation and functional maturation by upregulating synapsin expression in cortical and hippocampal neurons. However, it remains controversial whether BDNF affects synapsin expression in spinal cord anterior horn neurons. Wistar rat spinal cord anterior horn neurons were cultured in serum-supplemented medium containing BDNF, BDNF antibody, and Hank's solution for 3 days, and then synapsin I and synaptophysin protein and mRNA expression was detected. Under serum-supplemented conditions, the number of surviving neurons in the spinal cord anterior horn was similar among BDNF, anti-BDNF, and control groups (P > 0.05). Synapsin I and synaptophysin protein and mRNA expressions were increased in BDNF-treated neurons, but decreased in BDNF antibody-treated neurons (P < 0.01). These results indicated that BDNF significantly promotes synapsin I and synaptophysin expression in in vitro-cultured rat spinal cord anterior horn neurons.
基金Supported by The Canadian Institute of Health Research(CIHR)
文摘Synapsin Ⅱ is a member of the neuronal phosphoprotein family. These phosphoproteins are evolutionarily conserved across many organisms and are important in a variety of synaptic functions, including synaptogenesis and the regulation of neurotransmitter release. A number of genome-wide scans, meta-analyses, and genetic susceptibility studies have implicated the synapsin II gene(3p25) in the etiology of schizophrenia(SZ) and other psychiatric disorders. Further studies have found a reduction of synapsin II m RNA and protein in the prefrontal cortex in post-mortem samples from schizophrenic patients. Disruptions in the expression of this gene may cause synaptic dysfunction, which can result in neurotransmitter imbalances, likely contributing to the pathogenesis of SZ. SZ is a costly, debilitating psychiatric illness affecting approximately 1.1% of the world's population, amounting to 51 million people today. The disorder is characterized by positive(hallucinations, paranoia), negative(social withdrawal, lack of motivation), and cognitive(memory impairments, attention deficits) symptoms. This review provides a comprehensive summary of the structure, function, and involvement of the synapsin family, specifically synapsin II, in the pathophysiology of SZ and possible target for therapeutic intervention/implications.
基金Yunnan Provincial Department of Science and Technology Project(202101AY070001-224).
文摘Schizophrenia(SCZ)is the most common serious mental illness with a high disability rate and heavy social and family burdens.At present,there is no clear etiology and pathogenesis of schizophrenia.Studies have shown that the occurrence of schizophrenia may be related to the abnormality of the hypothalamic-pituitary-adrenal(HPA)axis.The LIM-homeobox gene 3(LHXS)and early growth response 1(EGR1)can affect pituitary function.Because the synapsin 2(SYN2)gene polymorphism regulates the activity of LHX3 and EGR1,it may cause the occurrence of schizophrenia.This article will review the possible involvement of SYN2 gene polymorphism in the pathogenesis of schizophrenia via regulating the activity of LHX3 and EGR1,then to afiect the HPA axis.
基金supported by the National Natural Science Foundation of China,Nos.81974358,81772453(to DSX)。
文摘Paired associative stimulation has been used in stroke patients as an innovative recovery treatment.However,the mechanisms underlying the therapeutic effectiveness of paired associative stimulation on neurological function remain unclear.In this study,rats were randomly divided into middle cerebral occlusion model(MCAO)and paired associated magnetic stimulation(PAMS)groups.The MCAO rat model was produced by middle cerebral artery embolization.The PAMS group received PAMS on days 3 to 20 post MCAO.The MCAO group received sham stimulation,three times every week.Within 18 days after ischemia,rats were subjected to behavioral experiments—the foot-fault test,the balance beam walking test,and the ladder walking test.Balance ability was improved on days 15 and 17,and the footfault rate was less in their affected limb on day 15 in the PAMS group compared with the MCAO group.Western blot assay showed that the expression levels of brain derived neurotrophic factor,glutamate receptor 2/3,postsynaptic density protein 95 and synapsin-1 were significantly increased in the PAMS group compared with the MCAO group in the ipsilateral sensorimotor cortex on day 21.Resting-state functional magnetic resonance imaging revealed that regional brain activities in the sensorimotor cortex were increased in the ipsilateral hemisphere,but decreased in the contralateral hemisphere on day 20.By finite element simulation,the electric field distribution showed a higher intensity,of approximately 0.4 A/m^2,in the ischemic cortex compared with the contralateral cortex in the template.Together,our findings show that PAMS upregulates neuroplasticity-related proteins,increases regional brain activity,and promotes functional recovery in the affected sensorimotor cortex in the rat MCAO model.The experiments were approved by the Institutional Animal Care and Use Committee of Fudan University,China(approval No.201802173 S)on March 3,2018.
基金supported by the National Natural Science Foundation of China,No.81601121,31500968the Natural Science Foundation of Jiangsu Province of China,No.BK20150163the Fundamental Research Fund for the Central Universities of China,No.JUSRP11567
文摘Impaired hippocampal neurogenesis is one of the early pathological features of Alzheimer's disease. Enhancing adult hippocampal neurogenesis has been pursued as a potential therapeutic strategy for Alzheimer's disease. Recent studies have demonstrated that environmental novelty activates β2-adrenergic signaling and prevents the memory impairment induced by amyloid-β oligomers. Here, we hypothesized that β2-adrenoceptor activation would enhance neurogenesis and ameliorate memory deficits in Alzheimer's disease. To test this hypothesis, we investigated the effects and mechanisms of action of β2-adrenoceptor activation on neurogenesis and memory in amyloid precursor protein/presenilin 1(APP/PS1) mice using the agonist clenbuterol(intraperitoneal injection, 2 mg/kg). We found that β2-adrenoceptor activation enhanced hippocampal neurogenesis, ameliorated memory deficits, and increased dendritic branching and the density of dendritic spines. These effects were associated with the upregulation of postsynaptic density 95, synapsin 1 and synaptophysin in APP/PS1 mice. Furthermore, β2-adrenoceptor activation decreased cerebral amyloid plaques by decreasing APP phosphorylation at Thr668. These findings suggest that β2-adrenoceptor activation enhances neurogenesis and ameliorates memory deficits in APP/PS1 mice.
基金supported by the National Natural Science Foundation of China(grant number 81273110)the Health Industry Research Special Funds for public welfare projects(grant number 201402021)the National Key Technology Research and Development Program(grant number 2014BAI12B02)
文摘Objective To investigate acrylamide(ACR)-induced subacute neurotoxic effects on the central nervous system(CNS) at the synapse level in rats. Methods 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. Results 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. Conclusion Subacute ACR exposure contributes to neuropathy in the rat CNS. Functional damage of synaptic proteins and vesicles may be a mechanism of ACR neurotoxicity.
