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Objective @#To investigate the protective effects and mechanisms of soybean phospholipid powder on nerve cells in vitro and rats neural tissues.@*Methods @#In the cell experiments , the cytotoxicity of soybean phospholipid powder with different concentrations on mouse microglia cells ( BV2 ) and rat adrenal pheochromocytoma (PC12) cells was ob served by cell counting kit⁃8( CCK⁃8) assay. The effect of soybean phospholipid powder on the NO level of BV2 cells was analyzed by NO determination experiment , and the synaptic growth of PC12 cells was observed under the microscope. In the animal experiment , the cognitive dysfunction of rat was simulated by scopol⁃ ocampal tissue morphology and nerve cell density of scopolamine model mice were ob served by hematoxylin ⁃eosin staining (HE) staining.@*Results @#Soybean phospholipid powder had no obvious cytotoxicity on BV2 cells and PC12 cells within the concentration of 1 000 μg/ml. Compared with the control group , the NO secretion of BV2 cells pretreated with soybean phospholipid powder significantly decreased (P < 0. 01) , and the neuronal synapse growth of PC12 cells significantly increased (P < 0. 01) . In comparison to the model group , soybean phospholipid powder significantly improved the learning and memory ability of scopolamine model rats (P < 0. 05) , reduced the neuronal damage in dentate gyrus (DG) , cornu ammonis3 (CA3) , cornu ammonis1 (CA1) areas of hippocampus , and increased the density of nerve cells (P < 0. 001) .@*Conclusion @#Soybean phospholipid powder can play a neuroprotective role by reducing neuroinflammation and promoting neuronal synapse growth at the cellular level , and improve the learning and memory ability of rats with cognitive impairment , reduce hippocampal tissue damage.
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Objective @#To study the effect of lipopolysaccharide ( LPS) -induced immune system activation on syn- aptic structure and DISC1. @*Methods @#40 rats were divided into 4 groups,which were PBS group,PBS + MK-801 group,LPS group and LPS + MK-801 group.The rats in LPS group and LPS + MK-801 group were administrated with LPS solution (0. 2 mg / kg,i.p.BIW) for 6 times in total, the rats in PBS group and PBS + MK801 group were administrated with PBS.At the third time when the rats were administrated with LPS solution,the rats in PBS + MK-801 group and LPS + MK-801 group were administrated with MK-801 solution (0. 5 mg / kg,i.p.BIW) for a total of 4 times,the rats in PBS group and LPS group were adminis- trated with saline.The head shaking and the open field tests were then evaluated in the rats.Immediately,the rats were sacrificed,and their brain were saved for testing. RT-qPCR , Golgi staining,immunohistochemistry and ELISA kits were used to detect DISC1 gene expression,dendritic spine status,microglia activation and inflammatory cytokine content in cortex,respectively. gene expression in the cortex of rats with schizophrenia.@*Results @# Compared with the PBS group,the expression of DISC1 gene of the rats in the PBS + MK-801 group increased (P <0. 01) ,the score of head shaking increased (P <0. 01) ,and the distance of the open field increased (P <0. 000 1) ; As well as the LPS + MK-801 group,compared with the LPS group,the expression of DISC1 gene increased (P<0. 000 1) ,the head shaking score and the distance of the open field increased (P<0. 000 1) . In addition,compared with the PBS + MK-801 group,the expression of DISC1 gene, the shaking head score and the open field distance of the LPS + MK-801 group further improved (P <0. 000 1) . Furthermore,compared with PBS group and PBS + MK-801 group,the content of iba1 in the cortex of LPS group and LPS + MK-801 group significantly increased (P <0. 05 ) ,the content of inflammatory cytokines significantly increased (P<0. 05) ,and the length and density of dendritic spines significantly decreased (P<0. 05) .@*Conclusion@#The activation of the immune system induced by LPS can contribute to the susceptibility of schizophrenia model, and the possible mechanism is that it cooperates with MK-801 to increase the expression of DISC1 gene,which ulti- mately leads to abnormal mental behavior in rats.
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ObjectiveTo investigate the mechanism of Dihuang Yinzi in improving astrocyte injury and protecting synaptic structure and function in the brain of Alzheimer's disease (AD) mice. MethodForty male APP/PS1 transgenic mice aged four months were randomly divided into a model group and a model + Dihuang Yinzi (0.25 g·kg-1) group, with 20 mice in each group. Forty C57BL/6J mice with the same background and same age were randomly divided into a control group and a control + Dihuang Yinzi (0.25 g·kg-1) group, with 20 mice in each group. The mice in the control + Dihuang Yinzi group and the model + Dihuang Yinzi group were administered with Dihuang Yinzi by gavage, and those in the control group and the model group received an equal volume of sterilized normal saline, once a day for 150 days. The learning and memory ability of mice was tested by the light-dark box test and Y-maze spontaneous alternation test. The content of glutamate (Glu) and glutamine (Gln) was measured by liquid chromatography-tandem mass spectrometry (LC-MS). Long-term potentiation (LTP) assay was used to detect synaptic plasticity in brain tissues. The protein expression levels of excitatory amino acid transporter 2 (EAAT2), postsynaptic density protein95 (PSD95), and synaptophysin (SYN) in brain tissues were measured by Western blot. Immunofluorescence was used to assess the localization and expression of EAAT2. Colorimetry was performed to detect Na+-K+ ATPase activity in mouse brain tissues. ResultAs compared with the control group, the model group showed shortened residence latency (P<0.01), increased number of errors (P<0.01) in the light-dark box test, reduced spontaneous alternation behaviors (P<0.01), no significant difference in the total number of arm entries in the Y-maze spontaneous alternation test, down-regulated expression of EAAT2, PSD95, and SYN (P<0.01), blunted activity of Na+-K+ ATPase (P<0.01), up-regulated Glu level (P<0.01), down-regulated Gln level (P<0.01), and reduced relative population spike (PS) amplitude and the slope of excitatory postsynaptic potential (EPSP) (P<0.05, P<0.01), while the above experimental indexes were not significantly different in the control + Dihuang Yinzi group. Compared with the model group, the model + Dihuang Yinzi group displayed prolonged residence latency (P<0.05), decreased number of errors (P<0.01) in the light-dark box test, increased spontaneous alternation behaviors (P<0.01), no significant difference in the total number of arm entries in the Y-maze spontaneous alternation test, up-regulated expression of EAAT2, PSD95, and SYN (P<0.01), potentiated activity of Na+-K+ ATPase (P<0.01), reduced Glu level (P<0.01), up-regulated Gln level (P<0.01), and increased PS amplitude and EPSP slope (P<0.01). ConclusionDihuang Yinzi can improve cognitive dysfunction in AD mice by protecting astrocytes, increasing Glu uptake to reduce its abnormal accumulation, and protecting synaptic structure and function.
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Abstract@#Alzheimer's disease (AD) is a neurodegenerative disease characterized by deposition of β-amyloid (Aβ). Liver X receptors (LXRs), a member of the nuclear receptor transcription factor superfamily, are widely expressed in brain, which may be involved in the development and progression of AD. Based on the international and national publications pertaining to the association between LXRs and AD from 2010 to 2022, this review summarizes the advances on the involvement of LXRs in the regulation of cholesterol metabolism, inflammatory response and synapse formation in the pathogenesis of AD was reviewed, so as to provide insights into the prevention and treatment of AD.
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Background Neurotransmitter secretion disorder induced by chronic manganese poisoning has always been one of the important causes of body injury, but the mechanism of neurotransmitter secretion disorder caused by manganese is not clear at present. Objective To investigate the effects of presynaptic membrane intracellular protein 13-1 (Munc13-1) and synapse fusion protein binding protein 18-1 (Munc18-1) on dopamine secretion dysfunction induced by manganese chloride (MnCl2) in human neuroblastoma (SH-SY5Y) cells. Methods A SH-SY5Y cell model induced by MnCl2 was established. Cell viability was measured by MTT assay. Four experimental groups were set up: control group and low-, medium-, and high-dose manganese groups (0, 100, 200, and 400 μmol·L−1 MnCl2). They were treated with corresponding doses of MnCl2 for 24 h. The secretion of dopamine was measured by enzyme-linked immunosorbent assay. The mRNA expression of Syntaxin-1 was detected by real-time quantitaive PCR. Total cell proteins were extracted, and the protein expression levels of Munc13-1, Munc18-1, and Syntaxin-1 were detected by Western blotting. The correlations of MnCl2 exposure and dopamine secretion with the protein expressions of Munc13-1 and Munc18-1 were also analyzed by Pearson correlation. Results Compared with the control group, the cell viability rate decreased gradually with the increase of manganese exposure concentration, and the difference between the medium- and the high-dose manganese groups was statistically significant (P<0.05). The concentration of dopamine in cell culture medium of all manganese exposure groups decreased with the increase of manganese concentration, and compared with the control group and the low-dose manganese group, the medium- and the high-dose manganese groups were statistically significant (P<0.05). The expression of Syntaxin-1 at mRNA or protein level did not change significantly among groups (P>0.05). Compared with the control group, the protein expression of Munc13-1 decreased and that of Munc18-1 increased with the increase of manganese concentration (P<0.05). Compared with the low-dose manganese group, the changes of Munc13-1 protein in the high-dose manganese group and Munc18-1 protein in the medium- and high-dose manganese groups had statistical significance (P<0.05). Compared with the medium-dose manganese group, the protein changes of Munc18-1 in the high-dose manganese group were statistically significant (P<0.05). The correlation analysis showed that MnCl2 dose was negatively correlated with Munc13-1 protein expression (r=−0.898, P<0.05), and positively correlated with Munc18-1 protein expression (r=0.678, P<0.05). Dopamine secretion was positively correlated with Munc13-1 protein expression (r=0.932, P<0.05), and negatively correlated with Munc18-1 protein expression (r=−0.817, P<0.05). Conclusion The inhibition of dopamine secretion in SH-SY5Y cells induced by manganese exposure is related to up-regulation of Munc18-1 and down-regulation of Munc13-1 expression levels, which may be one of the reasons for nerve injury caused by manganese.
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The physiological functions of endogenous amyloid-β (Aβ), which plays important role in the pathology of Alzheimer's disease (AD), have not been paid enough attention. Here, we review the multiple physiological effects of Aβ, particularly in regulating synaptic transmission, and the possible mechanisms, in order to decipher the real characters of Aβ under both physiological and pathological conditions. Some worthy studies have shown that the deprivation of endogenous Aβ gives rise to synaptic dysfunction and cognitive deficiency, while the moderate elevation of this peptide enhances long term potentiation and leads to neuronal hyperexcitability. In this review, we provide a new view for understanding the role of Aβ in AD pathophysiology from the perspective of physiological meaning.
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Humanos , Doença de Alzheimer/patologia , Peptídeos beta-Amiloides/metabolismo , Potenciação de Longa Duração , Transmissão Sináptica/fisiologia , HipocampoRESUMO
Brain size abnormality is correlated with an increased frequency of autism spectrum disorder (ASD) in offspring. Genetic analysis indicates that heterozygous mutations of the WD repeat domain 62 (WDR62) are associated with ASD. However, biological evidence is still lacking. Our study showed that Wdr62 knockout (KO) led to reduced brain size with impaired learning and memory, as well as ASD-like behaviors in mice. Interestingly, Wdr62 Nex-cKO mice (depletion of WDR62 in differentiated neurons) had a largely normal brain size but with aberrant social interactions and repetitive behaviors. WDR62 regulated dendritic spinogenesis and excitatory synaptic transmission in cortical pyramidal neurons. Finally, we revealed that retinoic acid gavages significantly alleviated ASD-like behaviors in mice with WDR62 haploinsufficiency, probably by complementing the expression of ASD and synapse-related genes. Our findings provide a new perspective on the relationship between the microcephaly gene WDR62 and ASD etiology that will benefit clinical diagnosis and intervention of ASD.
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Camundongos , Animais , Microcefalia/genética , Transtorno Autístico/metabolismo , Transtorno do Espectro Autista/metabolismo , Proteínas do Tecido Nervoso/metabolismo , Encéfalo/metabolismo , Camundongos Knockout , Proteínas de Ciclo Celular/metabolismoRESUMO
Aim To investigate the involvement of cy-clophilin D ( CypD ) -mediated mitochondrial permeability transition pore ( mPTP) in the neuroprotective effects of melatonin on cognitive impairment induced by repeated exposure to sevoflurane in newborn animals. Methods Mice were randomly assigned into control group, sevoflurane ( Sevo) group, and melatonin pre-treatment + sevoflurane ( Sevo + Mel) group. JC-1 kit was used to assess the mitochondrial membrane potential ( MMP) ; Western blot analysis was used to evaluate the protein expressions of CypD, postsynaptic density protein 95 ( PSD95 ), and Synapsin-1; and behavioral test were employed to measure cognitive function. Results The MMP level in the Sevo group was significantly reduced compared to the control group (P < 0. 01 ), the expression of CypD increased (P <0. 05), whereas the expression of PSD95 and Synapsin-1 decreased ( P < 0. 01) . Furthermore, the new object recognition index and spatial memory ability both exhibited a significant decline (P < 0. 01, P < 0. 05). However, when compared to the Sevo group, Sevo + Mel group could raise the MMP level (P <0. 01), increase the expression of synaptic proteins ( P < 0. 05 ), decrease the expression of CypD (P <0. 01) and elevate the new object recognition index and the spatial memory capacity ( P < 0. 01 ). Conclusions Melatonin could ameliorate cognitive impairment induced by repeated exposure to sevoflurane in newborn mice, and the underlying mechanism may be attributed to the inhibition of mPTP mediated by CypD and the promotion of synaptic protein synthesis.
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@#Studies suggest that synaptic damage is closely associated with cognitive dysfunction, and lemur tyrosine kinase 1 (LMTK1) is a key kinase that affects synaptic growth. Dihydroergotamine (DHE) is an ergot alkaloid derivative with high biological activity, which could regulate cognition, memory processing and motor control.This study aims to investigate the effect of DHE on synapse atrophy and plasticity as well as cognition in Alzheimer’s disease (AD) model animals.SAMR1 mice were selected as control group (n = 12).SAMP8 mice were randomly divided into 3 groups (n = 12 for each group):AD group, DHE low-dose group and high-dose group.The DHE groups were injected DHE intraperitoneally daily for 8 weeks.Immunofluorescence experiments, Golgi staining experiment, electrophysiological experiment, Morris water maze experiment (MWM) and Western blot experiment were conducted to investigate the effect of DHE on synaptic morphology, synaptic plasticity, cognitive function as well as the phosphorylation level of LMTK1 downstream TBC1D9B in AD model mice.Subsequently, the LMTK1 silencing and overexpression cells were constructed.Immunofluorescence experiments were used to study the effect of DHE on synaptic length of nerve cell after LMTK1 silencing and overexpression.In the hippocampus of AD mice, the postsynaptic marker PSD95 was significantly increased after DHE administration, which suggested that DHE could increase the synaptic density. In Golgi staining experiment, synaptic atrophy was observed in the hippocampal of AD mice, which could be improved by high-dose DHE.Compared with normal mice, the long-term potentiation (LTP) level of AD model mice was significantly reduced (P < 0.000 1), DHE could increase LTP significantly.The MWM experiment further showed that DHE could improve cognitive function in AD mice.WB experiments showed that the level of P-LMTK1 in the hippocampus of AD mice increased significantly, and the level of downstream P-TBC1D9B decreased significantly after DHE administration.Cell immunofluorescence experiments in vitro had shown that DHE significantly improved synaptic atrophy in overexpressed C17.2 cells, while its improvement disappeared when LMTK1 was silenced. This research suggests DHE may improve synaptic atrophy and cognitive dysfunction in AD by targeting on LMTK1.
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OBJECTIVE To study the effects of Dianxianqing granules on the tau protein in P301S mice by regulating mitophagy. METHODS Totally 36 P301S mice were randomly divided into model group, Dianxianqing granule group (12.48 g/kg), donepezil hydrochloride group (positive control, 1.3 mg/kg), with 12 mice in each group; another 10 C57BL6 mice were selected as control group. Administration groups were given relevant drug solutions intragastrically, and control group and model group were given constant volume of water intragastrically. The gavage volume was 20 mL/kg, once a day, for consecutive 5 months. During the experiment, the general condition of mice was observed in each group. After the last medication, the learning and memory ability was determined by Y maze test and Morris water maze test; HE staining was used to observe the morphological changes in brain tissue, and Nissl staining was used to observe the structure of neural cells and the number of Nissl bodies in cerebral tissue. Immunohistochemistry was used to detect the expressions of phospho-tau serine 202/threonine 205 (abbreviated as AT8) in brain tissue. Western blot assay was used to determine the expressions of mitophagy-associated proteins [PTEN-induced putative kinase-1 (PINK1), Parkin, microtubule-associated protein 1 light chain 3B (LC3B), p62], synaptic-associated proteins [postsynaptic density protein-95 (PSD-95), synaptophysin (SYP), and growth-associated protein-43 (GAP-43)] and the phosphorylation of tau protein [expressed by the phosphorylation levels of serine 199 (Ser199) and Ser202] in brain tissue. RESULTS The mice in E-mail:lnzyxyqy2003@163.com model group showed symptoms such as white hair, decreased body mass, and lower limb paralysis, with incomplete hippocampal structures in their brain tissue, as well as incomplete cell membrane edges and cell structures; the spontaneous alternating response rate, the times of crossing platform, the number of Nissl bodies, the protein expressions of PINK1, Parkin, LC3B, SYP, GAP-43, and PSD-95 were decreased significantly, compared with control group; swimming latency (fourth and fifth day), the protein expressions of AT8 and p62,the phosphorylation levels of Ser199 and Ser202 were increased or lengthened significantly, compared with control group (P<0.05 or P<0.01). Compared with model group, the above symptoms and indexes of mice were improved significantly in administration groups (P<0.05 or P<0.01). CONCLUSIONS Dianxianqing granules can effectively improve cognitive impairment in P301S mice,the mechanism of which may be associated with inducing mitochondrial autophagy, reducing the hyperphosphorylation of tau protein, up-regulating the expression of synaptic-associated proteins in brain tissue,and repairing damaged neural cells.
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ObjectiveTo construct a neural network-like tissue with the potential of synaptic formation in vitro by seeding human induced pluripotent stem cell-derived neural precursor cells (hiPSC-NPCs) on decellularized optic nerve (DON), so as to provide a promising approach for repair of nerve tissue injury. MethodsThrough directional induction and tissue engineering technology, human induced pluripotent stem cells (hiPSCs) and 3D DON scaffolds were combined to construct neural network-like tissues. Then the hiPSCs were directionally induced into human neural precursor cells (hNPCs) and neurons. Immunofluorescence staining was used to identify cell differentiation efficiency. 3D DON scaffolds were prepared. Morphology and cytocompatibility of scaffolds were identified by scanning electron microscopy and Tunnel staining. Induced hiPSC-NPCs were seeded on DON scaffolds. Immunofluorescence staining, scanning electron microscopy, transmission electron microscopy and patch clamp were used to observe the morphology and functional identification of constructed neural network tissues. Results①The results of immunofluorescence staining suggested that most of hiPSC-NPCs differentiated into neurons in vitro. We had successfully constructed a neural network dominated by neurons. ② The results of scanning electron microscopy and immunohistochemistry suggested that a neural network-like tissue with predominating excitatory neurons in vitro was successfully constructed. ③The results of immunohistochemical staining, transmission electron microscopy and patch clamp indicated that the neural network-like tissue had synaptic transmission function. ConclusionA neural network-like tissue mainly composed of excitatory neurons has been constructed by the combination of natural uniform-channel DON scaffold and hiPSC-NPCs, which has the function of synaptic transmission. This neural network plays a significant role in stem cell derived replacement therapy, and offers a promising prospect for repair of spinal cord injury (SCI) and other neural tissue injuries.
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The bionic optic nerve can mimic human visual physiology and is a future treatment for visual disorders. Photosynaptic devices could respond to light stimuli and mimic normal optic nerve function. By modifying (Poly(3,4-ethylenedioxythio-phene):poly (styrenesulfonate)) active layers with all-inorganic perovskite quantum dots, with an aqueous solution as the dielectric layer in this paper, we developed a photosynaptic device based on an organic electrochemical transistor (OECT). The optical switching response time of OECT was 3.7 s. To improve the optical response of the device, a 365 nm, 300 mW·cm -2 UV light source was used. Basic synaptic behaviors such as postsynaptic currents (0.225 mA) at a light pulse duration of 4 s and double pulse facilitation at a light pulse duration of 1 s and pulse interval of 1 s were simulated. By changing the way light stimulates, for example, by adjusting the intensity of the light pulses from 180 to 540 mW·cm -2, the duration from 1 to 20 s, and the number of light pulses from 1 to 20, the postsynaptic currents were increased by 0.350 mA, 0.420 mA, and 0.466 mA, respectively. As such, we realized the effective shift from short-term synaptic plasticity (100 s recovery of initial value) to long-term synaptic plasticity (84.3% of 250 s decay maximum). This optical synapse has a high potential for simulating the human optic nerve.
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Humanos , Pontos Quânticos , Biônica , Óxidos , Nervo ÓpticoRESUMO
Human brain cholesterol acts as structural components of cellular membrane, synapse and dendrite formation.Researchers have found a possible association between low serum cholesterol levels and mood disorders though the literature from India in this regard is limited. To estimate serum levels of total cholesterol in patients with major depressive disorder. 75 patients of MDD were compared with equal number of age and sex matched controls. 5 ml of fasting sample of blood was obtained in a plain vacutainer to analyse total cholesterol level by Cholesterol oxidase-peroxidase method. Statistical analysis: The obtained results were tabulated and analyzed by multiple logistic regression analysis, independent t-test, Chi-square test and area under the curve. The mean level of cholesterol in cases (158.85±61.22 mg/dL) which was significantly lower compared to the controls (182.71±40.98 mg/dL) with P <0.01. The symptoms of MDD negatively correlated with lower serum cholesterol level with odds ratio of 0.99. There was statistically significant lower level of cholesterol in the MDD group below 140 mg/dL compared to the control group with P <0.001. As the measurement of total serum cholesterol is simple and cost effective, it can be used as an important biochemical marker for MDD.
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This paper aim is to discuss and clarify about the way we perceived the functionality of the synapse since 4th century BC up to modern times and actual status. The discussions over the way synapses work began over 2400 years ago and it all started from the simple question of how the locomotive system works and how do the muscles contract. The rst who discussed about this concept was Plato during the 4th century BC. We are discussing about René Descartes (1596-1650) depiction of a clear view in the book entitled “De Homine” (1662) over the view of the brain and the innervation of the body. In modern times, the word “synapse” was coined for the rst time in Michael Foster's 7th Edition “Textbook of Physiology” of 1897 , for which Sherrington wrote 3 chapters. He proposed his former Professor to introduce the word “synapse” which comes from Greek and means “conjunction”. For this discovery, Charles Sherrington and Edgar Douglas Adrian were awarded the Nobel Prize in Physiology or Medicine in 1932.
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Recent studies have revealed great functional and structural heterogeneity in the ribbon-type synapses at the basolateral pole of the isopotential inner hair cell (IHC). This feature is believed to be critical for audition over a wide dynamic range, but whether the spatial gradient of ribbon morphology is fine-tuned in each IHC and how the mitochondrial network is organized to meet local energy demands of synaptic transmission remain unclear. By means of three-dimensional electron microscopy and artificial intelligence-based algorithms, we demonstrated the cell-wide structural quantification of ribbons and mitochondria in mature mid-cochlear IHCs of mice. We found that adjacent IHCs in staggered pairs differ substantially in cell body shape and ribbon morphology gradient as well as mitochondrial organization. Moreover, our analysis argues for a location-specific arrangement of correlated ribbon and mitochondrial function at the basolateral IHC pole.
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Animais , Camundongos , Inteligência Artificial , Cóclea/metabolismo , Células Ciliadas Auditivas Internas , Mitocôndrias , Sinapses/metabolismoRESUMO
During the development of visual cortex, the structure of neurons will adaptively change and adjust according to the changes of external environment, which shows structural plasticity.The experience-dependent plasticity of visual cortex is based on the structural changes of neurons, which mainly include change of synaptic connections, disappearance or increase of dendritic spines, turnover of dendritic spines, changes in the size of dendritic spines, changes in postsynaptic density and alterations of perineuronal nets.The structural changes of neurons have significant influence on the plasticity of visual cortex function and structure, and are highly associated with some molecules or non-neuronal components such as paired immunoglobulin-like receptor B, Ly-6/neurotoxin-like protein 1, Nogo, microglia and extracellular matrix and so on.In addition, external intervention factors such as abnormal visual experience and environmental enrichment can have significant impact on the regulation of the structural changes of neurons, and finally influence the development of visual function and the recovery from visual impairment.In comparison with the functional studies, studies on the structural plasticity of visual cortical neurons depend on the state-of-the-art imaging techniques at cellular or sub-cellular level with more visualizable and convincing results.The constant exploration of the structural plasticity of visual cortex will enhance our understanding of visual development-related diseases, such as amblyopia, and lay the foundation for related basic research and innovative treatments.Advances in the structural plasticity of visual cortex were reviewed in this article.
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Objective:To explore the effect of enriched environment on pain sensitivity, anxiety- and depressive-like behavior in selective nerve injury(SNI) rats model and its potential mechanism.Methods:A total of 36 male clean grade SD rats aged 6-8 weeks were randomly divided into three groups( n=12 in each group): sham operation+ standard environment group (sham group), SNI+ standard environment group (standard environment group), SNI+ enriched environment group (enriched environment group). The rat model of neuropathic pain was established by SNI.The rats in the enriched enviroment group were placed in an enriched enviroment 7 days before operation until 21 days after operation.The paw withdraw threshold(PWT) and paw withdraw latency (PWL) were performed to assess hyperalgesia.The open field test, elevated plus maze test, novelty suppressed feeding test and forced swimming test were used to assess anxiety and depression like behavior.The expressions of cAMP response element binding protein (CREB), p-CREB, brain-derived neurotrophic factor (BDNF), postsynaptic density-95 (PSD-95) and neuroligin 2 (NLGN2) were detected by Western blot.The expression of CREB and BDNF in contralateral ACC were measured by immunofluorescence.GraphPad prism 8.0 and SPSS 23.0 were used for data analysis.One way ANOVA was used for inter group comparison, repeated measurement ANOVA was used to analyze PWT and PWL results, and Tukey test was used for pairwise comparison. Results:(1) In PWT and PWL experiments, the interaction effect between group and time, group main effect and time main effect of PWT were significant ( F=13.4, 39.6, 369.6, all P<0.05), and the interaction effect between group and time, group main effect and time main effect of PWL were significant ( F=3.8, 10.3, 58.8, all P<0.05). Compared with sham group, PWT((8.0±3.5) g, (2.4±1.4) g, (2.3±1.1) g, (2.2±1.6) g, (1.6±0.5) g) and PWL((8.6±1.3) s, (7.3±1.5) s, (7.9±1.0) s, (6.6±1.1) s, (7.7±1.4) s) in standard environment group decreased at each time point (all P<0.05). (2) Compared with sham group, the number of entrying into the central area (1.3±1.7), the time of entrying into the central area((1.6±1.3) s), the proportion of entering open arms ((8.0±7.8) %) and the proportion of time in the open arms ((1.3±1.2) %) all significantly decreased in standard environment group ( t=4.585, 5.423, 4.682, 5.202, all P<0.05). The eating latency ((365.2±94.4) s) and immobility time ((127.6±24.3) s) dramatically increased ( t=6.008, 14.290, both P<0.05). The number and time of entrying into central area of enriched environment group were both higher than those of standard environment group(both P<0.05), while the eating latency and immobility time of enriched environment group were both lower than those of standard environment group(both P<0.05). (3) Compared with sham group(CREB: (1.6±0.2), (0.8±0.5); BDNF: (0.8±0.5), (1.0±0.4)), the expression of CREB ((1.8±0.1), (1.5±0.2)), BDNF ((0.9±0.6), (1.4±0.3)) in spinal cord and ACC of standard environment group increased (spinal: t=3.283, 4.989; ACC: t=5.502, 4.257, all P<0.05). The expression of PSD-95 ((1.6±0.2), (1.0±0.2) and NLGN2 ((1.5±0.5), (1.1±0.2)) also increased in ACC of standard enviroment group ( t=4.257, 2.214, both P<0.05). Compared with standard environment group, the expression of CREB (1.3±0.3), BDNF (0.7±0.4), PSD-95(1.0±0.3) and NLGN2(1.1±0.4) in spinal cord of enriched environment group decreased ( t=5.007, 2.166, 2.358, 2.322, all P<0.05). The expression of PSD-95(1.2±0.3) and NLGN2(1.1±0.2) also decreased in ACC of enriched environment group ( t=2.674, 2.944, both P<0.05). However, the expression of p-CREB (1.7±0.6) and BDNF (2.4±0.2) increased in ACC ( t=4.180, 7.610, P<0.05). Conclusion:Enriched environment can improve neuropathic pain and anxiety- and depressive-like behavior in SNI rats, which may be related to the change of synaptic plasticity in spinal cord and ACC.
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ObjectiveTo observe the effect of Wenyang Jieyu decoction (WYJY) on the hippocampal structure of depressed rats with kidney-yang deficiency. MethodThe 105 SD rats were randomly divided into normal group, model group, fluoxetine group (4.17 mg·kg-1), Xiaoyaosan group (1.88 g·kg-1), and low-, medium- and high-dose (1.25,2.50,5.00 g·kg-1) WYJY groups,15 in each group. The depression model was induced by subcutaneous injection of corticosterone in rats except for those in the normal group and the rats were orally administered once a day for 28 days. The depression-like behaviors of rats were observed by sucrose preference test, novelty-suppressed feeding test, forced swimming test, and open field test. The morphology of hippocampal neurons was observed by hematoxylin-eosin(HE) staining, and the density of hippocampal neurons was detected by Nissl staining. The ultrastructure of hippocampal synapses was observed by transmission electron microscopy (TEM). The expression of synaptophysin (SYP), postsynaptic density-95 (PSD95), and apoptosis-related protein Caspase-3 in hippocampal neurons was observed by immunohistochemistry, and bromodeoxyuridine (BrdU) and doublecortin (DCX) were used to observe the apoptosis and regeneration of hippocampal neurons. ResultWYJY could improve weight loss in depressed rats. As revealed by the behavioral tests, the model group showed depression-like behaviors, which were relieved in the WYJY groups and the positive drug groups. HE staining showed that the nuclei of hippocampal neurons in the model group were constricted, deeply stained, and sparsely arranged, while the neurons in the WYJY groups and the positive drug groups were significantly improved. Nissl staining demonstrated that the cell density of the model group was lower than that of the normal group (P<0.05). Compared with model group, the groups with drug intervention showed increased cell density (P<0.05) and compact arrangement. According to the results in TEM, compared with normal group, the model group showed shortened synaptic active zone (P<0.05), widened synaptic cleft (P<0.05), and thinned tight zone (P<0.05). Compared with model group, the groups with drug intervention showed shortened synaptic active zone (P<0.05), narrowed synaptic cleft (P<0.05), and thickened tight zone (P<0.05). As displayed by the results of immunocytochemistry and immunofluorescence, compared with the normal group, the model group showed decreased protein expression of SYP, PSD95, BrdU, and DCX in the hippocampus (P<0.05) and increased protein expression of Caspase-3 (P<0.05). Compared with the model group, the groups with drug intervention showed increased protein expression of SYP, PSD95, BrdU, and DCX in the hippocampus (P<0.05) and decreased protein expression of Caspase-3 (P<0.05). ConclusionWYJY can promote the regeneration of hippocampal neurons in rats and improve the depression of rats.
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Objective To study the effect of velvet antler polypeptides (VAP) on Rho/ROCK pathway in APP/ PSl double transgenic mice. Methods APP/PSl double transgenic mice were randomly divided into model group and velvet antler polypeptide group, 20 mice in each group, and control group consisting of 20 mice of the same litter and the same gender negative. The mice in VAP group were given velvet antler polypeptide 100 mg/kg by intragastric administration once a day for 28 days. After treatment, the water maze experiment was detected and recorded the escape latency and the number of crossing platforms of the mice; the ultrastructures of the synapse were observed by transmission electron microscopy; the expression of Rhs homolog gene family member A(RhoA) and Rho associated coiled-coil forming protein kinase II(ROCKII) in the hippocampal CAI area were observed by immunofluorescence. The expression levels of RhoA and ROCKII protein in the hippocampus were detected by Western blotting. The contents of hippocampus amyloid (3-protein(A(3),
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The central nervous system controls high-level neural activities such as perception, movement, language, and cognition. As the most important part of the human nervous system, its normaldevelopment and functional activities are very important in the process of human development. A betterunderstanding of the essential molecular pathways that regulate the development of the nervous systemmay improve diagnoses and treatments for neurologic diseases, as well as basic biological understanding ofthe brain. The dynamic changes of the modified state of RNA N