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Molecular evolution of Na^(+) channels in teleost fishes

Integrative Zoology 2009年第1期4卷 64-74页

作者： Harold H.ZAKON Manda C.JOST Derrick J.ZWICKL Ying LU David M.HILLIS section of neurobiology section of Integrative Biology The University of TexasAustinTXUSA

Voltage-dependent sodium channels are critical for electrical excitability.Invertebrates possess a single sodium channel gene;two rounds of genome duplication early in vertebrates increased the number to four.Since the teleost-tetrapod split,independent gene duplications in each lineage have further increased the number of sodium channel genes to 10 in tetrapods and 8 in teleosts.Here we review how the occurrence of multiple sodium channel paralogs has influenced the evolutionary history of three groups of fishes:pufferfish,gymnotiform and mor-myriform electric fish.Pufferfish(tetraodontidae)produce a neurotoxin,tetrodotoxin,that binds to and blocks the pore of sodium channels.Pufferfish evolved resistance to their own toxins by amino acid substitutions in the pore of their sodium channels.These substitutions had to occur in parallel across multiple paralogs for organismal re-sistance to evolve.Gymnotiform and mormyriform fishes independently evolved electric organs to generate elec-tricity for communication and object localization.Two sodium channel genes are expressed in muscle in most fishes.In both groups of weakly electric fishes,one gene lost its expression in muscle and became compartmen-talized in the evolutionary novel electric organ,which is a muscle derivative.This gene then evolved at elevated rates,whereas the gene that is still expressed in muscle does not show elevated rates of evolution.In the electric organ-expressing gene,amino acid substitutions occur in parts of the channel involved in determining how long the channel will be open or closed.The enhanced rate of sequence evolution of this gene likely underlies the spe-cies-level variations in the electric signal.

关键词： electric fish molecular evolution pufferfish sodium channels tetrodotoxin.

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Unraveling the mechanisms of synapse formation and axon regeneration: the awesome power of C. elegans genetics

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Science China(Life Sciences) 2015年第11期58卷 1084-1088页

作者： JIN YiShi Howard Hughes Medical Institute Section of Neurobiology Division of Biological Sciences University of California

Since Caenorhabditis elegans was chosen as a model organism by Sydney Brenner in 1960's, genetic studies in this organism have been instrumental in discovering the function of genes and in deciphering molecular signaling network. The small size of the organism and the simple nervous system enable the complete reconstruction of the first connectome. The stereotypic developmental program and the anatomical reproducibility of synaptic connections provide a blueprint to dissect the mechanisms underlying synapse formation. Recent technological innovation using laser surgery of single axons and in vivo imaging has also made C. elegans a new model for axon regeneration. Importantly, genes regulating synaptogenesis and axon regeneration are highly conserved in function across animal phyla. This mini-review will summarize the main approaches and the key findings in understanding the mechanisms underlying the development and maintenance of the nervous system. The impact of such findings underscores the awesome power of C. elegans genetics.

关键词：轴突再生突触形成遗传学线虫机制模式生物神经系统信号网络

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An update on spinal cord injury research

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Neuroscience Bulletin 2013年第4期29卷 399-401页

作者： Yimin Zou Neurobiology Section Biological Sciences Division University of California San Diego

Spinal cord injury （SCI） is an ever-increasing challenge. Severe injury can cause long-term loss of sensory and motor functions, as well as other chronic conditions, such as neuropathic pain and autonomic dysreflexia. So far, most research has been focused on acute injury. However, due to the lack of treatment, more and more individuals with this condition enter a chronic state, to which very little research effort has been dedicated.

关键词： An update on spinal cord injury research SCI

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Decorin treatment of spinal cord injury

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Neural Regeneration Research 2014年第18期9卷 1653-1656页

作者： Maryam Esmaeili Martin Berry Ann Logan Zubair Ahmed Neurotrauma Research Group Neurobiology SectionSchool of Clinical and Experimental MedicineUniversity of Birmingham

The scarring response after a penetrant central nervous system injury results from the interaction between invading leptominingeal/pericyte-derived fibroblasts and endogenous reactive astrocytes about the wound margin. Extracellular matrix and scar-derived axon growth inhibitory mole- cules fill the lesion site providing both a physical and chemical barrier to regenerating axons. Dec orin, a small leucine-rich chondroitin-dermatan sulphate proteoglycan expressed by neurons and astrocytes in the central nervous system, is both anti-fibrotic and anti-inflammatory and attenu- ates the formation and partial dissolution of established and chronic scars. Here, we discuss the potential of using Decorin to antagonise scarring in the central nervous system.

关键词： spinal cord injury Decorin transforming growth factor-beta scarring chondroiti^sulphate proteoglycan matrix metalloproteases

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Neuroprotective action of lithium in disorders of the central nervous system

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中南大学学报（医学版） 2011年第6期36卷 461-475页

作者： Chi-Tso CHIU De-Maw CHUANG section on Molecular neurobiology National Institute of Mental HealthNational Institutes of Health

Substantial in vitro and in vivo evidence of neurotrophic and neuroprotective effects of lithium suggests that it may also have considerable potential for the treatment of neurodegenerative conditions.Lithium's main mechanisms of action appear to stem from its ability to inhibit glycogen synthase kinase-3 activity and also to induce signaling mediated by brain-derived neurotrophic factor.This in turn alters a wide variety of downstream effectors,with the ultimate effect of enhancing pathways to cell survival.In addition,lithium contributes to calcium homeostasis.By inhibiting N-methyl-D-aspartate receptor-mediated calcium influx,for instance,it suppresses the calcium-dependent activation of pro-apoptotic signaling pathways.By inhibiting the activity of phosphoinositol phosphatases,it decreases levels of inositol 1,4,5-trisphosphate,a process recently identified as a novel mechanism for inducing autophagy.These mechanisms allow therapeutic doses of lithium to protect neuronal cells from diverse insults that would otherwise lead to massive cell death.Lithium,moreover,has been shown to improve behavioral and cognitive deficits in animal models of neurodegenerative diseases,including stroke,amyotrophic lateral sclerosis,fragile X syndrome,and Huntington's,Alzheimer's,and Parkinson's diseases.Since lithium is already FDA-approved for the treatment of bipolar disorder,our conclusions support the notion that its clinical relevance can be expanded to include the treatment of several neurological and neurodegenerative-related diseases.

关键词：《中南大学学报:医学版》期刊摘要编辑部

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Mesenchymal stem cell therapy for retinal ganglion cell neuroprotection and axon regeneration

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Neural Regeneration Research 2015年第3期10卷 371-373页

作者： Ben Mead Ben A.Scheven Neurotrauma Research Group Neurobiology SectionSchool of Clinical and Experimental MedicineUniversity of Birmingham School of Dentistry University of Birmingham

Retinal ganglion cells （RGCs） are responsible for propagat- ing signals derived from visual stimuli in the eye to the brain, along their axons within the optic nerve to the superior colliculus, lateral geniculate nucleus and visu- al cortex of the brain. Damage to the optic nerve either through trauma, such as head injury, or degenerative dis- ease, such as glaucoma causes irreversible loss of function through degeneration of non-regenerating RGC axons and death of irreplaceable RGCs, ultimately leading to blindness （Berry et al., 2008）. The degeneration of RGCs and their axons is due to the loss of the necessary source of retrogradely transported neurotrophic factors （NTFs） being hindered by axonal injury. NTFs are survival factors for neurons and play a pivotal part in axon regeneration. Stem cells particularly mesenchymal stem cells （MSCs） have been shown to possess a natural intrinsic capacity for paracrine support, releasing multiple signalling mol- ecules including NTFs. By transplanting MSCs into the vitreous, they are positioned adjacent to the injured reti- na to provide paracrine-mediated therapy for the retinal neuronal cells （Johnson et al., 2010a; Mead et al., 2013）. Additionally, MSCs may be pre-differentiated into sup- portive glial-like cells, such as Schwann cells, which could further increase their potential for paracrine support of injured neurons （Martens et al., 2013）. Thus, MSCs have received considerable attention as a new cellular therapy for both traumatic and degenerative eye disease, acting as an alternative source of NTFs, protecting injured RGCs and promoting regeneration of their axons （Figure 1）.

关键词： DPSCs RGCs BMSCs stem Mesenchymal stem cell therapy for retinal ganglion cell neuroprotection and axon regeneration cell

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Effects of(-)stepholidine in animal models for schizophrenia

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Acta Pharmacologica Sinica 2006年第9期27卷 1111-1118页

作者： Bart A ELLENBROEK 6500 HB Nijmegen Department of Cognitive Neurosciences section Molecular neurobiology The Netherlands University of Nijmegen

Aim:(-)Stepholidine(SPD)is an active ingredient of the Chinese herb Stephaniaintermedia,which binds to the dopamine D1and D2like receptors.Biochemical,electrophysiological and behavioural experiments have provided strong evidencethat SPD is both a D1and a D2antagonist,which could make SPD a uniqueantipsychotic drug.The present study aimed to investigate the antipsychoticproperties of SPD in two animal models for schizophrenia.Methods:The effectsof SPD,clozapine and haloperidol in increasing forelimb and hindlimb retractiontime in the paw test and in reversing the apomorphine and MK801-induced dis-ruption of prepulse inhibition was investigated.Results:In the paw test,clozapineand SPD increased the hindlimb retraction time,with only a marginal effect on theforelimb retraction time,whereas haloperidol potently increased both.In theprepulse inhibition paradigm,all three drugs reverse the apomorphine-induceddisruption in prepulse inhibition,while none of the drugs could reverse the MK801-induced disruption.SPD even slightly,but significantly,potentiated the effectsof MK801.Conclusion:The data show that SPD showed antipsychotic-like ef-fects in both the prepulse inhibition paradigm and in the paw test.Moreover,theresults of the paw test suggest that SPD has an atypical character with a relativelysmall potency to induce extrapyramidal side effects.

关键词： acoustic startle response antipsyehotics apomorphine dopamine D1 receptor dopamine D2 receptor MK801 paw test prepulse inhibition clozapine haloperidol

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Emerging role of microRNAs in lipid metabolism

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Acta Pharmaceutica Sinica B 2015年第2期5卷 145-150页

作者： Zhihong Yang Tyler Cappello Li Wang Department of Physiology and neurobiology and the Institute for Systems Genomics University of Connecticut Veterans Affairs Connecticut Healthcare System Department of Internal Medicine Section of Digestive Diseases Yale University

micro RNAs(mi RNAs or mi Rs) are small non-coding RNAs that are involved in posttranscriptional regulation of their target genes in a sequence-specific manner. Emerging evidence demonstrates that mi RNAs are critical regulators of lipid synthesis, fatty acid oxidation and lipoprotein formation and secretion. Dysregulation of mi RNAs disrupts gene regulatory network, leading to metabolic syndrome and its related diseases. In this review, we introduced epigenetic and transcriptional regulation of mi RNAs expression. We emphasized on several representative mi RNAs that are functionally involved into lipid metabolism, including mi R-33/33 n, mi R122, mi R27a/b, mi R378/378 n, mi R-34 a and mi R-21.Understanding the function of mi RNAs in lipid homeostasis may provide potential therapeutic strategies for fatty liver disease.

关键词： Lipid metabolism microRNAs Nuclear receptors

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Impact of Pitx3 gene knockdown on glial cell line-derived neurotrophic factor transcriptional activity in dopaminergic neurons

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Neural Regeneration Research 2017年第8期12卷 1347-1351页

作者： Jing Chen Xiao-yu Kang Chuan-xi Tang Dian-shuai Gao Experiment Teaching Center of Morphology Xuzhou Medical University Xuzhou Jiangsu Province China Teaching and Research section of neurobiology and Anatomy Xuzhou Medical University Xuzhou Jiangsu Province China

Pitx3 is strongly associated with the phenotype, differentiation, and survival of dopaminergic neurons. The relationship between Pitx3 and glial cell line-derived neurotrophic factor（GDNF） in dopaminergic neurons remains poorly understood. The present investigation sought to construct and screen a lentivirus expression plasmid carrying a rat Pitx3 short hairpin（sh）RNA and to assess the impact of Pitx3 gene knockdown on GDNF transcriptional activity in MES23.5 dopaminergic neurons. Three pairs of interference sequences were designed and separately ligated into GV102 expression vectors. These recombinant plasmids were transfected into MES23.5 cells and western blot assays were performed to detect Pitx3 protein expression. Finally, the most effective Pitx3 sh RNA and a dual-luciferase reporter gene plasmid carrying the GDNF promoter region（GDNF-luciferase） were cotransfected into MES23.5 cells. Sequencing showed that the synthesized sequences were identical to the three Pitx3 interference sequences. Inverted fluorescence microscopy revealed that the lentivirus expression plasmids carrying Pitx3-sh RNA had 40-50% transfection efficiency. Western blot assay confirmed that the corresponding Pitx3 of the third knockdown sequence had the lowest expression level. Dual-luciferase reporter gene results showed that the GDNF transcriptional activity in dopaminergic cells cotransfected with both plasmids was decreased compared with those transfected with GDNF-luciferase alone. Together, the results showed that the designed Pitx3-sh RNA interference sequence decreased Pitx3 protein expression, which decreased GDNF transcriptional activity.

关键词： nerve regeneration neurodegeneration Parkinson＇s disease glial cell line-derived neurotrophic .factor Pitx3 MES23.5 cells shorthairpin RNA gene knockdown plasmid dual-luciferase reporter gene neural regeneration

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Carboxypeptidase E (NF-α1):a new trophic factor in neuroprotection

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Neuroscience Bulletin 2014年第4期30卷 692-696页

作者： Yong Cheng Niamh X.Cawley Y.Peng Loh section on Cellular neurobiology Program on Developmental NeuroscienceEunice Kennedy Shriver National Institute of Child Health and Human DevelopmentNational Institutes of Health BethesdaMD 20892USA

Carboxypeptidase E （CPE） is a prohormone-processing enzyme and sorting receptor that functions intracellularly. However, recent studies have demonstrated that CPE acts as atrophic factor extracellularly to up-regulate the expression of a pro-survival gene. This mini-review summarizes the roles of CPE in neuroprotection and the implications for neurodegenerative diseases.

关键词： carboxypeptidase E NF-α1 neuroprotection stress neurodegenerative disease

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