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Loss of autoreceptor functions in mice lacking the dopamine transporter

NATURE NEUROSCIENCE 1999年第7期2卷 649-655页

作者： Jones, SR Gainetdinov, RR Hu, XT Cooper, DC Wightman, RM White, FJ Caron, MG Duke Univ Med Ctr Dept Cell Biol Howard Hughes Med Inst Durham NC 27710 USA Finch Univ Hlth Sci Chicago Med Sch N Chicago IL 60064 USA Univ N Carolina Dept Chem Chapel Hill NC 27599 USA Univ N Carolina Curriculum Neurobiol Chapel Hill NC 27599 USA

Autoreceptors provide an important inhibitory feedback mechanism for dopamine neurons by altering neuronal functions in response to changes in extracellular levels of dopamine. Elevated dopamine may be a component of several neuropsychiatric disorders. However, evidence concerning the state of autoreceptors in such conditions has remained elusive. The function of dopamine autoreceptors was assessed in mice lacking the dopamine transporter (DAT). Genetic deletion of the DAT gene in mice results in a persistent elevation in levels of extracellular dopamine. Direct assessment of impulse-, synthesis- and release-regulating autoreceptors in these mice reveals a nearly complete loss of function. These findings may provide insight into the neurochemical consequences of hyperdopaminergia.

关键词： 3 4-二羟苯酰乙酸/代谢放射自显影术脑/生理学载体蛋白质类/遗传学载体蛋白质类/生理学多巴胺/代谢多巴胺激动剂/药代动力学多巴胺质膜转运蛋白质类电刺激反馈/生理学基因缺失高香草酸/代谢碘放射性同位素膜糖蛋白类膜转运蛋白质类中脑/代谢小鼠近交C57BL 小鼠基因敲除微透析神经组织蛋白质类/缺乏神经组织蛋白质类/生理学神经元/药物作用神经元/生理学喹吡罗/药理学受体多巴胺D2/代谢水杨酰胺类/药代动力学动物小鼠

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(Over)correction of FMR1 deficiency with YAC transgenics: behavioral and physical features

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HUMAN MOLECULAR GENETICS 2000年第8期9卷 1145-1159页

作者： Peier, AM McIlwain, KL Kenneson, A Warren, ST Paylor, R Nelson, DL Baylor Coll Med Dept Mol & Human Genet Houston TX 77030 USA Emory Univ Sch Med Dept Chem Atlanta GA 30322 USA Emory Univ Sch Med Howard Hughes Med Inst Atlanta GA 30322 USA

Fragile X syndrome is a common cause of mental retardation involving loss of expression of the FMR1 gene. The role of FMR1 remains undetermined but the protein appears to be involved in RNA metabolism. Fmr1 knock-out mice exhibit a phenotype with some similarities to humans, such as macroorchidism and behavioral abnormalities. As a step toward understanding the function of FMR1 and the determination of the potential for therapeutic approaches to fragile X syndrome, yeast artificial chromosome (YAC) transgenic mice were generated in order to determine whether the Fmr1 knockout mouse phenotype could be rescued. Several transgenic lines were generated that carried the entire FMR1 locus with extensive amounts of flanking sequence. We observed that the YAC transgene supported production of the human protein (FMRP) which was present at levels 10 to 15 times that of endogenous protein and was expressed in a cell- and tissue-specific manner. Macroorchidism was absent in knockout mice carrying the YAC transgene indicating functional rescue by the human protein. Given the complex behavioral phenotype in fragile X patients and the mild phenotype previously reported for the Fmr1 knockout mouse, we performed a more thorough evaluation of the Fmr1 knockout phenotype using additional behavioral assays that had not previously been reported for this animal model. The mouse displayed reduced anxiety-related responses with increased exploratory behavior. FMR1 YAC transgenic mice overexpressing the human protein did produce opposing behavioral responses and additional abnormal behaviors were also observed. These findings have significant implications for gene therapy for fragile X syndrome since overexpression of the gene may harbor its own phenotype.

关键词：脑/代谢染色体人工酵母外显子脆性X智力低下蛋白质脆性X综合征/遗传学脆性X综合征/治疗基因疗法精神障碍/遗传学小鼠基因敲除小鼠转基因运动活动神经组织蛋白质类/缺乏神经组织蛋白质类/遗传学神经组织蛋白质类/生理学表型 RNA结合蛋白质类重组蛋白质类/生物合成睾丸/代谢动物人类男(雄)性小鼠

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Aberrant development of motor axons and neuromuscular synapses in erbB2-deficient mice

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PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA 2000年第3期97卷 1299-1304页

作者： Lin, WC Sanchez, HB Deerinck, T Morris, JK Ellisman, M Lee, KF Salk Inst Biol Studies La Jolla CA 92037 USA Univ Calif San Diego Natl Ctr Microscopy & Imaging Res Dept Neurosci La Jolla CA 92093 USA

Receptor tyrosine kinase erbB2, which is activated by neuregulin, is expressed in Schwann and muscle cells in the developing neuromuscular junction (NMJ). in vitro studies have shown that neuregulin promotes the survival and migration of Schwann cells and stimulates acetylcholine receptor gene transcription in cultured muscle cells. These findings suggest an important role for erbB2 in the development of the NMJ. Here we examine erbB2-deficient mice to determine whether erbB2 is required for NMJ development in vivo. Our analysis shows that there are pre- and postsynaptic defects of developing NMJ in erbB2-deficient embryos. The presynaptic defects include defasciculation and degeneration of the motor nerves, and an absence of Schwann cells. The postsynaptic defect features an impairment of junctional folds at the neuromuscular synapse in the mutants. These results demonstrate that erbB2 is essential for in vivo development of the NMJ.

关键词：轴突/病理学细胞运动膈/胚胎学膈/病理学胚胎和胎儿发育基因表达调控发育期基因 erbB-2 原位杂交荧光肋间肌/胚胎学肋间肌/病理学小鼠基因敲除小鼠神经学突变型形态发生运动神经元/病理学肌蛋白质类/缺乏肌蛋白质类/遗传学肌蛋白质类/生理学神经变性神经组织蛋白质类/缺乏神经组织蛋白质类/遗传学神经组织蛋白质类/生理学神经调节蛋白类/生理学神经肌肉接头/畸形神经肌肉接头/胚胎学膈神经/胚胎学膈神经/病理学受体 erbB-2/缺乏受体 erbB-2/生理学受体胆碱能/生物合成受体胆碱能/遗传学许旺细胞/代谢许旺细胞/病理学动物小鼠

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Deficits in memory and motor performance in synaptotagmin IV mutant mice

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PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA 2000年第10期97卷 5598-5603页

作者： Ferguson, GD Anagnostaras, SG Silva, AJ Herschman, HR Univ Calif Los Angeles Inst Mol Biol Los Angeles CA 90095 USA Univ Calif Los Angeles Dept Biol Chem Los Angeles CA 90095 USA Univ Calif Los Angeles Dept Neurobiol Los Angeles CA 90095 USA Univ Calif Los Angeles Dept Psychiat Los Angeles CA 90095 USA Univ Calif Los Angeles Dept Psychol Los Angeles CA 90095 USA Univ Calif Los Angeles Dept Pharmacol Los Angeles CA 90095 USA Univ Calif Los Angeles Brain Res Inst Los Angeles CA 90095 USA

Synaptotagmin (Syt) TV is a synaptic vesicle protein. Syt IV expression is induced in the rat hippocampus after systemic kainic acid treatment. To examine the functional role of this protein in vivo, we derived Syt IV null [Syt IV(-/-)] mutant mice. Studies with the rotorod revealed that the Syt IV mutants have impaired motor coordination, a result consistent with constitutive Syt IV expression in the cerebellum. Because Syt IV is thought to modulate synaptic function, we also have examined Syt IV mutant mice in learning and memory tests. Our studies show that the Syt IV mutation disrupts contextual fear conditioning, a learning task sensitive to hippocampal and amygdala lesions. In contrast, cued fear conditioning is normal in the Syt IV mutants, suggesting that this mutation did not disrupt amygdala function. Conditioned taste aversion, which also depends on the amygdala, is normal in the Syt IV mutants. Consistent with the idea that the Syt IV mutation preferentially affects hippocampal function, Syt IV mutant mice also display impaired social transmission of food preference. These studies demonstrate that Syt IV is critical for brain function and suggest that the Syt IV mutation affects hippocampal-dependent reaming and memory, as well as motor coordination.

关键词：声刺激钙结合蛋白质类条件反射经典/生理学提示恐惧/生理学偏食纯合子行走膜糖蛋白类/缺乏膜糖蛋白类/遗传学膜糖蛋白类/生理学记忆/生理学记忆障碍/遗传学小鼠基因敲除运动活动/遗传学运动活动/生理学神经组织蛋白质类/缺乏神经组织蛋白质类/遗传学神经组织蛋白质类/生理学反射社会行为突触结合蛋白质类味觉动物小鼠大鼠

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Live or let die -: retinal ganglion cell death and survival during development and in the lesioned adult CNS

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TRENDS IN NEUROSCIENCES 2000年第10期23卷 483-490页

作者： Bähr, M Univ Tubingen Neurol Klin D-72076 Tubingen Germany

Programmed cell death or apoptosis is a common and widespread phenomenon that is important for proper development of the nervous system. In the adult CNS, however, apoptosis contributes to secondary cell loss after various types of lesions. The retino-tectal system has been successfully used as a convenient model system to study the molecular mechanisms of neuronal apoptosis and survival during development and in the lesioned adult CNS. This review describes the current knowledge about the interactions of cell death and survival pathways in general and for retinal ganglion cells specifically.

关键词：细胞凋亡/生理学凋亡蛋白酶活化因子1 脑损伤/病理学脑源性神经营养因子/药理学脑源性神经营养因子/生理学秀丽新小杆线虫/细胞学秀丽新小杆线虫/胚胎学秀丽新小杆线虫/生长和发育载体蛋白质类/遗传学载体蛋白质类/生理学半胱氨酸天冬氨酸蛋白酶/缺乏半胱氨酸天冬氨酸蛋白酶/遗传学半胱氨酸天冬氨酸蛋白酶/生理学细胞存活基因 bcl-2 蠕虫蛋白质类/生理学小鼠基因敲除线粒体/生理学形态发生神经组织蛋白质类/缺乏神经组织蛋白质类/遗传学神经组织蛋白质类/生理学蛋白质类/遗传学蛋白质类/生理学原癌基因蛋白质类/缺乏原癌基因蛋白质类/遗传学原癌基因蛋白质类/生理学原癌基因蛋白质c-bcl-2/缺乏原癌基因蛋白质c-bcl-2/遗传学原癌基因蛋白质c-bcl-2/生理学视网膜/细胞学视网膜/胚胎学视网膜/生长和发育视网膜神经节细胞/细胞学视网膜神经节细胞/代谢视网膜神经节细胞/病理学 bcl-2相关X蛋白质 bcl相关死亡蛋白质 bcl-X蛋白质成年人动物鸡胚人类小鼠

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FMRP involvement in formation of synapses among cultured hippocampal neurons

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CEREBRAL CORTEX 2000年第10期10卷 1045-1052页

作者： Braun, K Segal, M Weizmann Inst Sci Dept Neurobiol IL-76100 Rehovot Israel Leibniz Inst Neurobiol D-39008 Magdeburg Germany

Fragile-X, the main cause of inherited human mental retardation is associated with the absence of a recently identified fragile-X mental retardation protein (FMRP). Mice in which this protein is lacking due to a knockout (KO) mutation are reported to express altered dendritic spines on their cortical neurons compared with wild type (WT) controls. We have used tissue-cultured neurons to examine differences in morphology and synaptic connectivity between WT and FMRP-deficient mice. Hippocampal neurons taken from KO mice and grown in culture for 3 weeks have shorter dendrites and fewer dendritic spines than their WT counterparts. Also, KO cells tend to express fewer functional synaptic connections, which develop more slowly and produce smaller excitatory synaptic currents than WT controls. These observations may have important implications for the understanding of mental retardation associated with the absence of FMRP.

关键词：细胞培养的树突/超微结构电生理学脆性X智力低下蛋白质海马/细胞学海马/病理学海马/生理学海马/超微结构小鼠近交系小鼠基因敲除/遗传学神经组织蛋白质类/缺乏神经组织蛋白质类/遗传学神经组织蛋白质类/生理学神经元/生理学神经元/超微结构 RNA结合蛋白质类参考值突触/生理学突触/超微结构动物小鼠

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Enhanced association of mutant triosephosphate isomerase to red cell membranes and to brain microtubules

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PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA 2000年第3期97卷 1026-1031页

作者： Orosz, F Wágner, G Liliom, K Kovács, J Baróti, K Horány, M Farkas, T Hollán, S Ovádi, J Hungarian Acad Sci Biol Res Ctr Inst Enzymol H-1518 Budapest Hungary Eotvos Lorand Univ Fac Sci Dept Gen Zool H-1445 Budapest Hungary Natl Inst Haematol & Immunol H-1113 Budapest Hungary Hungarian Acad Sci Inst Biochem Biol Res Ctr H-6701 Szeged Hungary

In a Hungarian family with triosephosphate isomerase (TPI;D-glyceraldehyde-3-phosphate keto-isomerase, EC 5.3.1.1) deficiency, two germ-line identical, but phenotypically differing compound heterozygote brothers tone of them with neurological disorder) have been identified with the same very low (< 5%) TPI activity and 20- or 40-fold higher erythrocyte dihydroxyacetone phosphate levels as compared with normal controls. Our present studies with purified TPI and hemolysates revealed the binding of TPI, and the binding of human wild-type and mutant TPIs in hemolysate, to the red cell membrane, and the interference of binding with other hemolysate proteins. The binding of the mutant TPI is enhanced as compared with the wild-type enzyme. The increased binding is influenced by both the altered structure of the mutant and the changes in the red cell membrane. Compared with binding of glyceraldehyde-3-phosphate dehydrogenase, the isomerase binding is much less sensitive to ionic strength or blocking of the N-terminal tail of the band-3 transmembrane protein. The binding of TPIs to the membrane decreases the isomerase activity, resulting in extremely high dihydroxyacetone phosphate levels in deficient cells. In cell-free brain extract, tubulin copolymerizes with TPI and with other cytosolic proteins forming highly decorated microtubules as shown by immunoblot analysis with anti-TPI antibody and by electron microscopic images. The efficacy order of TPI binding to microtubules is propositus > brother without neurological disorder > normal control. This distinct microcompartmentation of mutant proteins may be relevant in the development of the neurodegenerative process in TPI deficiency and in other, more common neurological diseases.

关键词：贫血溶血性先天性/酶学贫血溶血性先天性/遗传学基底神经节疾病/酶学基底神经节疾病/遗传学结合竞争性生物转运脑/酶学细胞膜/代谢密码子/遗传学二羟丙酮磷酸/代谢红细胞/酶学杂合子大分子物质微管/酶学神经组织蛋白质类/缺乏神经组织蛋白质类/遗传学神经组织蛋白质类/代谢点突变蛋白质结合终止区遗传丙糖磷酸异构酶/缺乏丙糖磷酸异构酶/遗传学丙糖磷酸异构酶/代谢微管蛋白/代谢动物牛人类男(雄)性大鼠

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Ablation of P/Q-type Ca²⁺ channel currents, altered synaptic transmission, and progressive ataxia in mice lacking the α_1A-subunit

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PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA 1999年第26期96卷 15245-15250页

作者： Jun, K Piedras-Renteria, ES Smith, SM Wheeler, DB Lee, SB Lee, TG Chin, HM Adams, ME Scheller, RH Tsien, RW Shin, HS Pohang Univ Sci & Technol Natl Creat Res Initiat Ctr Calcum & Learning Pohang 790784 South Korea Pohang Univ Sci & Technol Dept Life Sci Pohang 790784 South Korea Stanford Univ Sch Med Dept Mol & Cellular Physiol Stanford CA 94305 USA Stanford Univ Sch Med Howard Hughes Med Inst Stanford CA 94305 USA NIH Genet Res Branch Div Neurosci & Basic Behav Sci Bethesda MD 20892 USA Univ Calif Riverside Dept Entomol Riverside CA 92521 USA Univ Calif Riverside Dept Neurosci Riverside CA 92521 USA

The Ca2+ channel alpha(1A)-subunit is a voltage-gated, pore-forming membrane protein positioned at the intersection of two important lines of research: one exploring the diversity of Ca2+ channels and their physiological roles, and the other pursuing mechanisms of ataxia, dystonia, epilepsy, and migraine. alpha(1A)-Subunits are thought to support both P- and Q-type Ca2+ channel currents, but the most direct test, a null mutant, has not been described, nor is it known which changes in neurotransmission might arise from elimination of the predominant Ca2+ delivery system at excitatory nerve terminals. We generated alpha(1A)-deficient mice (alpha(1A)(-/-)) and found that they developed a rapidly progressive neurological deficit with specific characteristics of ataxia and dystonia before dying approximate to 3-4 weeks after birth. P-type currents in Purkinje neurons and P- and Q-type currents in cerebellar granule cells were eliminated completely whereas other Ca2+ channel types, including those involved in triggering transmitter release, also underwent concomitant changes in density. Synaptic transmission in alpha(1A)(-/-) hippocampal slices persisted despite the lack of P/Q-type channels but showed enhanced reliance on N-type and R-type Ca2+ entry. The alpha(1A)(-/-) mice provide a starting point for unraveling neuropathological mechanisms of human diseases generated by mutations in alpha(1A).

关键词：共济失调钙/代谢钙通道/缺乏钙通道/遗传学钙通道 N型钙通道 P型/代谢钙通道 Q型/代谢小脑/代谢导电性海马/代谢小鼠基因敲除神经组织蛋白质类/缺乏神经组织蛋白质类/遗传学神经系统疾病/病因学浦肯野细胞/代谢突触传递动物小鼠

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No obvious abnormality in mice deficient in receptor protein tyrosine phosphatase β

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MOLECULAR AND CELLULAR BIOLOGY 2000年第20期20卷 7706-7715页

作者： Harroch, S Palmeri, M Rosenbluth, J Custer, A Okigaki, M Shrager, P Blum, M Buxbaum, JD Schlessinger, J NYU Med Ctr Dept Pharmacol New York NY 10016 USA NYU Med Ctr Skirball Inst New York NY 10016 USA NYU Med Ctr Dept Physiol & Neurosci New York NY 10016 USA Univ Rochester Med Ctr Dept Neurobiol & Anat Rochester NY 14642 USA CUNY Mt Sinai Sch Med Dept Neurobiol New York NY 10029 USA CUNY Mt Sinai Sch Med Dept Psychiat New York NY 10029 USA

The development of neurons and glia is governed by a multitude of extracellular signals that control protein tyrosine phosphorylation, a process regulated by the action of protein tyrosine kinases and protein tyrosine phosphatases (PTPs), Receptor PTP beta (RPTP beta;also known as PTP zeta) is expressed predominantly in the nervous system and exhibits structural features common to cell adhesion proteins, suggesting that this phosphatase participates in cell-cell communication. It has been proposed that the three isoforms of RPTP beta play a role in regulation of neuronal migration, neurite outgrowth, and gliogenesis. To investigate the biological functions of this PTP, we have generated mice deficient in RPTP beta. RPTP beta-deficient mice are viable, are fertile, and showed no gross anatomical alterations in the nervous system or other organs. In contrast to results of in vitro experiments, our study demonstrates that RPTP beta is not essential for neurite outgrowth and node formation in mice, The ultrastructure of nerves of the central nervous system in RPTP beta-deficient mice suggests a fragility of myelin, However, conduction velocity was not altered in RPTP beta-deficient mice. The normal development of neurons and glia in RPTP beta-deficient mice demonstrates that RPTP beta function is not necessary for these processes in vivo or that loss of RPTP beta can be compensated for by other PTPs expressed in the nervous system.

关键词：印迹法 DNA 脑/细胞学脑/代谢脑/超微结构细胞黏附分子神经元细胞运动导电性基因缺失基因打靶免疫印迹法免疫组织化学同工酶类/缺乏同工酶类/遗传学同工酶类/代谢小鼠基因敲除显微镜检查电子髓鞘/代谢神经组织蛋白质类/缺乏神经组织蛋白质类/遗传学神经组织蛋白质类/代谢神经元/细胞学神经元/代谢神经元/超微结构视神经/生理学视神经/超微结构表型蛋白质酪氨酸磷酸酶类/缺乏蛋白质酪氨酸磷酸酶类/遗传学蛋白质酪氨酸磷酸酶类/代谢 RNA 信使/代谢受体样蛋白质酪氨酸磷酸酶类 5类受体细胞表面/代谢钠通道/代谢动物小鼠

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Abnormal neurotransmission in mice lacking synaptic vesicle protein 2A (SV2A)

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PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA 1999年第26期96卷 15268-15273页

作者： Crowder, KM Gunther, JM Jones, TA Hale, BD Zhang, HZ Peterson, MR Scheller, RH Chavkin, C Bajjalieh, SM Univ Washington Dept Pharmacol Seattle WA 98195 USA Univ Washington Dept Psychol Seattle WA 98195 USA Stanford Univ Dept Mol & Cellular Physiol Stanford CA 94305 USA Stanford Univ Howard Hughes Med Inst Stanford CA 94305 USA

Synaptic vesicle protein 2 (SV2) is a membrane glycoprotein common to all synaptic and endocrine vesicles. Unlike many proteins involved in synaptic exocytosis, SV2 has no homolog in yeast, indicating that it performs a function unique to secretion in higher eukaryotes. Although the structure and protein interactions of SV2 suggest multiple possible functions, its role in synaptic events remains unknown. To explore the function of SV2 in an in vivo context, we generated mice that do not express the primary SV2 isoform, SV2A, by using targeted gene disruption. Animals homozygous for the SV2A gene disruption appear normal at birth. However, they fail to grow, experience severe seizures, and die within 3 weeks, suggesting multiple neural and endocrine deficits, Electrophysiological studies of spontaneous inhibitory neurotransmission in the CA3 region of the hippocampus revealed that loss of SV2A leads to a reduction in action potential-dependent gamma-aminobutyric acid (GABA)ergic neurotransmission. In contrast, action potential-independent neurotransmission was normal. Analyses of synapse ultrastructure suggest that altered neurotransmission is not caused by changes in synapse density or morphology. These findings demonstrate that SV2A is an essential protein and implicate it in the control of exocytosis.

关键词：脑/解剖学和组织学内分泌系统/畸形基因致死海马/生理学纯合子膜糖蛋白类/缺乏膜糖蛋白类/遗传学小鼠基因敲除/生长和发育诱变神经组织蛋白质类/缺乏神经组织蛋白质类/遗传学神经系统畸形蛋白质亚型发作/遗传学突触/超微结构突触传递/生理学 γ氨基丁酸/代谢动物小鼠

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