首页 | 本学科首页   官方微博 | 高级检索  
文章检索
  按 检索   检索词:      
出版年份:   被引次数:   他引次数: 提示:输入*表示无穷大
  收费全文   2789篇
  免费   125篇
  国内免费   56篇
  2023年   65篇
  2022年   62篇
  2021年   88篇
  2020年   58篇
  2019年   77篇
  2018年   64篇
  2017年   59篇
  2016年   35篇
  2015年   64篇
  2014年   89篇
  2013年   129篇
  2012年   97篇
  2011年   94篇
  2010年   75篇
  2009年   111篇
  2008年   131篇
  2007年   135篇
  2006年   131篇
  2005年   89篇
  2004年   126篇
  2003年   90篇
  2002年   101篇
  2001年   67篇
  2000年   70篇
  1999年   66篇
  1998年   59篇
  1997年   50篇
  1996年   57篇
  1995年   62篇
  1994年   56篇
  1993年   47篇
  1992年   41篇
  1991年   50篇
  1990年   45篇
  1989年   49篇
  1988年   37篇
  1987年   24篇
  1986年   29篇
  1985年   22篇
  1984年   24篇
  1982年   23篇
  1981年   20篇
  1980年   14篇
  1979年   13篇
  1978年   17篇
  1977年   12篇
  1976年   9篇
  1973年   9篇
  1971年   8篇
  1970年   6篇
排序方式: 共有2970条查询结果,搜索用时 15 毫秒
881.
In order to determine the ongoing role of retinal fibers in the development of dorsal lateral geniculate nucleus (dLGN) neurons during postnatal development, the development of dLGN neurons in the postnatal absence of retinal input was studied in pigmented ferrets using the Golgi-Hortega technique. The development of four dLGN cell classes, defined on the basis of somatic and dendritic morphology, was described previously in normal ferrets (Sutton and Brunso-Bechtold, 1991, J. Comp. Neurol. 309 : 71–85). The present results indicate that the morphological development of dLGN neurons is strikingly similar in normal and experimental ferrets. The exuberant dendritic appendages that appear after eye opening in normal ferrets are overproduced and eliminated in the postnatal absence of retinal input; however, the final reduction of these transient appendages is delayed. Because exuberant appendages develop in the absence of retinal input, their production cannot depend upon visual experience. Differences in cell body size between normal and experimental ferrets are apparent only after neurons can be classified at the end of the first postnatal month. Cell body size is markedly reduced for class 1 neurons; class 2 cells also are reduced in size but to a far lesser extent. As there is a general trend for class 1 neurons to have the functional properties of Y-cells, it is likely that the dLGN neurons most affected by the absence of retinal input also are Y-cells. © 1993 John Wiley & Sons, Inc.  相似文献   
882.
883.
《Cell》2021,184(23):5715-5727.e12
  1. Download : Download high-res image (133KB)
  2. Download : Download full-size image
  相似文献   
884.
《Cell reports》2020,30(6):2028-2039.e4
  1. Download : Download high-res image (140KB)
  2. Download : Download full-size image
  相似文献   
885.
Quantitative and morphometric observations were carried out on neurons of L3-L6 dorsal root ganglia (DRGs) in control and vitamin-E-deficient rats at different ages. Controls were fed a standard diet and sacrificed at 1 or at 5 months of age; deficient rats were fed a diet without vitamin E from 1 to 5 months of age and then sacrificed. No significant difference in total number of neurons was found, but an increase in neuron sizes, a decrease in nucleus-cytoplasm ratio, and a more circular neuron shape were found in controls with increasing age (from 1 to 5 months). In L3-L6 DRGs of vitamin-E-deficient rats (5 months of age), a higher number of neurons was found than in those of either young or adult controls. Moreover, some morphometric characteristics of neurons in the deficient rats were similar to those of neurons in 1-month-old controls. The findings suggest that vitamin E deficiency can trigger events resulting in appearance of new neurons, possibly anticipating phenomena that normally occur in aging.  相似文献   
886.
887.
888.
889.
《Current biology : CB》2020,30(22):4541-4546.e5
  1. Download : Download high-res image (123KB)
  2. Download : Download full-size image
  相似文献   
890.
Sound production that is mediated by intrinsic or extrinsic swim bladder musculature has evolved multiple times in teleost fishes. Sonic muscles must contract rapidly and synchronously to compress the gas‐filled bladder with sufficient velocity to produce sound. Muscle modifications that may promote rapid contraction include small fiber diameter, elaborate sarcoplasmic reticulum (SR), triads at the A–I boundary, and cores of sarcoplasm. The diversity of innervation patterns indicate that sonic muscles have independently evolved from different trunk muscle precursors. The analysis of sonic motor pathways in distantly related fishes is required to determine the relationships between sonic muscle evolution and function in acoustic signaling. We examined the ultrastructure of sonic and adjacent hypaxial muscle fibers and the distribution of sonic motor neurons in the coral reef Pyramid Butterflyfish (Chaetodontidae: Hemitaurichthys polylepis) that produces sound by contraction of extrinsic sonic muscles near the anterior swim bladder. Relative to adjacent hypaxial fibers, sonic muscle fibers were sparsely arranged among the endomysium, smaller in cross‐section, had longer sarcomeres, a more elaborate SR, wider t‐tubules, and more radially arranged myofibrils. Both sonic and non‐sonic muscle fibers possessed triads at the Z‐line, lacked sarcoplasmic cores, and had mitochondria among the myofibrils and concentrated within the peripheral sarcoplasm. Sonic muscles of this derived eutelost possess features convergent with other distant vocal taxa (other euteleosts and non‐euteleosts): small fiber diameter, a well‐developed SR, and radial myofibrils. In contrast with some sonic fishes, however, Pyramid Butterflyfish sonic muscles lack sarcoplasmic cores and A–I triads. Retrograde nerve label experiments show that sonic muscle is innervated by central and ventrolateral motor neurons associated with spinal nerves 1–3. This restricted distribution of sonic motor neurons in the spinal cord differs from many euteleosts and likely reflects the embryological origin of sonic muscles from hypaxial trunk precursors rather than occipital somites. J. Morphol., 2013. © 2012 Wiley Periodicals, Inc.  相似文献   
设为首页 | 免责声明 | 关于勤云 | 加入收藏

Copyright©北京勤云科技发展有限公司  京ICP备09084417号