Reticulocyte transfer RNA and hemoglobin synthesis
Reticulocyte transfer RNA and hemoglobin synthesis
复制标题
网织红细胞转移RNA和血红蛋白合成
作者：
D. W. Smith
范围从5 × 10-'到2 × 10- m，体积从0.13到0.04 ul，没有局部麻醉作用的证据。在14只动物中，有9只动物在向黑质注入安非他明后，尾状壳核的神经元放电增加，而在4只动物中未受影响，在1只动物中尾状壳核的活动下降。将安非他命注入黑质上方的网状结构，或致密部以下黑质的网状部分，通常会导致这些结构中记录电极的神经元活动增加，尽管也看到相反的情况，并且神经元活动增加通常伴随着尾状壳核记录部位的这些变化。目前尚不清楚在这种情况下，尾状壳核神经元放电的增加是由于多巴胺能抑制的释放，还是由于黑质或网状结构中非多巴胺能成分的活性增加，两者都可以进入尾状壳核（51）。Bunney等人（31）报道，静脉注射安非他明对多巴胺能神经元放电的抑制作用可通过在安非他明给药前15至30分钟用dl -t-甲基酪氨酸（一种抑制儿茶酚胺合成的药物）治疗而被阻断。斯派特，A. Sjoerdsma， S. Udenfriend， J. Pharmacol。试析，147,86 (1965)；M. J. Besson， A. Cheramy， J. Glowinski，同上，177,196 (1971)；Weissman et al.[15]。我们也可以用类似的预处理方法减少或消除局部输注安非他明对多巴胺能神经元放电的抑制（N = 4）。此外，这种化合物通常会导致黑质致密部和尾壳核的自发神经元活动显著增加。53. B. S. Bunney和G. K. Aghajanian，《儿茶酚胺研究的前沿》，E. Usdin和S. Snyder主编。（佩加蒙，纽约，1973年），第961页。54. 轴突横断似乎确实阻止安非他明诱导的多巴胺从新纹状体多巴胺能终端释放[M]。J. Besson， A. Cheramy， C. Gauchy， J. Glowinski, NaunynSchmiedebergs Arch。中华医学杂志，1998,11 (3)；Von Voightlander和Moore (19)]， U. Ungerstedt[在The Neurosciences， Third Study Program， F. 0]中提出了轴突横断对完整轴突侧枝末端释放儿茶酚胺的类似阻断作用。施密特和F. G.沃登主编。（麻省理工学院出版社，剑桥，马萨诸塞州）， 1974)，第9791页。55. J. Parizek， R. Hassler， I. J. Bak, Zellforsch。Mikrosk。《论文集》，115,137（1971）。56. R. J. Naylor和J. E. Olley，神经药理学11,91 (1972)；B.科斯塔尔和R. J.内勒，欧洲。医学杂志，25,121 (1974)；S. Wolfarth, Pharmacol。物化学。行为，2,181（1974）。57. T. Arnfred和A. Randrup, Acta Pharmacol。中国生物医学工程杂志，1999,19 (2)；A. Randrup和1。Munkvad，《安非他命及其相关化合物国际研讨会》，E. Costa和S. Garattini主编。（乌鸦出版社，纽约，1970年），第695页。58. R. C. Duvoisin, Arch。神经病学杂志，17,124（1967）。59. js。Kim和R. Hassler, Brain Res. 88,150（1975）。60. W. Rail， G. M. Shepherd， T. S. Reese， M. W. Brightman, Exp. Neurol. 14,44 (1966)；D. D.惠勒，L. L.博雅尔斯基，W. H.布鲁克斯，J.塞尔。物理学报，67,141 (1966)；H. J. Ralston III，J。神经科杂志，132,275 (1968)；R. D. Lund，同上135,179 (1969)；j·e·道林，《投资》眼科杂志，9,655 (1970)；A. Van Harreveld and E. Fifkova， J.神经生物学杂志，2,13 (1970)；李志强，陈志强。中华神经医学杂志，1999,11 (1)；B. N. Harding, Brain Res. 34,181 (1971)；D. K.莫瑞斯特，Z.阿纳特。Entwicklungsgesch. 133, 216 (1971)；h·j·拉尔斯顿，《自然》230,585 (1971)；G. M. Shepherd, Brain Res. 32, 212 (1971)；J. J.斯洛珀，同上34,186 (1971)；E. V. Famiglietti, Jr.和A. Peters，J。神经科杂志，144,285 (1972)；G. W. Kreutzberg和L. Toth，自然科学，61,37 (1974)；A. Van Harreveld and E. Fifkova, Brain Res. 81,455 (1974)；M. A.盖耶，W. J.道西，A. J.曼德尔，同上85,135 (1975)；P.舒伯特和G. W.克罗伊茨伯格，同上90,319 (1975)；D. Weinreich和R. Hammerschlag，同上，84,137（1975）。61. J. F. R. Koenig和R. A. Klippel，《大鼠脑：前脑和脑干下部的立体定位图谱》（Williams & Wilkins, Baltimore, 1963）。62. 部分由NIMH基金MH 19515和研究科学家发展奖K02 MH 70706（给P.M.G.）支持。我们还感谢卫生、教育和福利部向科罗拉多大学研究生院提供的生物医学科学支持赠款，用于购买贝克曼气体分析仪，并感谢史密斯克莱恩和法国实验室提供硫酸d-安非他明。我们感谢P. Wilson熟练的技术协助，P. Dawson协助准备手稿，以及J. Groves绘制插图。我们感谢圣地亚哥加利福尼亚大学医学院的D. S. Segal和科罗拉多大学的H. Alpern、E. Fifkova、R. MacGregor、K. Schlesinger和S. Sharpless的帮助和建议。
ranging from 5 x 10-' to 2 x 10-4M and volumes from 0.13 to 0.04 ul, without evidence of local anesthetic effects. In 9 of 14 animals, neuronal firing in the caudate-putamen increased following infusion of amphetamine into the substantia nigra, while in four animals it was unaffected and in one animal activity declined in the caudate-putamen. Infusion of amphetamine into the reticular formation above the substantia nigra, or in pars reticulata of the substantia nigra below pars compacta, usually resulted in increased neuronal activity at the recording electrode in these structures, although the reverse was also seen, and increased neuronal activity typically accompanied these changes at the recording site in the caudate-putamen. It is unclear whether in such instances increased neuronal firing in the caudate-putamen is due to release from dopaminergic inhibition, or increased activity in nondopaminergic elements of the substantia nigra or reticular formation, both of which have access to the caudate-putamen (51). Bunney et al. (31) have reported that the inhibition of dopaminergic neuronal firing produced by intravenously administered amphetamine can be blocked by treatment 15 to 30 minutes prior to amphetamine administration with DL-t-methyl-ptyrosine, a drug that inhibits synthesis of catecholamines [S. Spector, A. Sjoerdsma, S. Udenfriend, J. Pharmacol. Exp. Ther. 147, 86 (1965); M. J. Besson, A. Cheramy, J. Glowinski, ibid. 177, 196 (1971); Weissman et al. (15)]. We have also been able to reduce or abolish the depression of dopaminergic neuronal firing produced by local infusion of amphetamine with similar pretreatments (N = 4). In addition, this compound typically leads to marked increases in spontaneous neuronal activity in both pars compacta of the substantia nigra and the caudate-putamen. 53. B. S. Bunney and G. K. Aghajanian, in Frontiers in Catecholamine Research, E. Usdin and S. Snyder, Eds. (Pergamon, New York, 1973), p. 961. 54. Axonal transection does appear to block amphetamine-induced release of dopamine from dopaminergic terminals in the neostriatum [M. J. Besson, A. Cheramy, C. Gauchy, J. Glowinski, NaunynSchmiedebergs Arch. Pharmakol. 278, 101 (1973); Von Voightlander and Moore (19)] and a similar blocking effect of axonal transection on catecholamine release from terminals of intact axon collaterals has been suggested by U. Ungerstedt [in The Neurosciences, Third Study Program, F. 0. Schmitt and F. G. Worden, Eds. (MIT Press, Cambridge, Mass., 1974), p. 9791. 55. J. Parizek, R. Hassler, I. J. Bak, Z. Zellforsch. Mikrosk. Anat. 115, 137 (1971). 56. R. J. Naylor and J. E. 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We also acknowledge the support of the biomedical sciences support grant to the Graduate School of the University of Colorado from the Department of Health, Education, and Welfare for the purchase of the Beckman gas analyzer, and Smith Kline& French Laboratories for supplying the d-amphetamine sulfate. We thank P. Wilson for skilled technical assistance, P. Dawson for assistance in preparing the manuscript, and J. Groves for drawing the illustrations. We acknowledge the help and advice of D. S. Segal of the University of California Medical School at San Diego and H. Alpern, E. Fifkova, R. MacGregor, K. Schlesinger, and S. Sharpless of the University of Colorado.