课题基金 / 基金详情

项目摘要

项目成果

GUY A PERKINS的其他基金

相似基金

相关文献

中文摘要
翻译
点击翻译按钮获取中文摘要
英文摘要
This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. The basic structure, biochemistry and function of mammalian retinal rod and cone photoreceptors are well described. However, there are relatively few reports on the ultrastructural details of rod and cone mitochondria and even fewer on their comparative aspects. The 3-D technique with the highest resolution available for studying mitochondria is electron microscope tomography. Comparative studies of structure related to function offer a promising means of understanding the significance of differences in cytoarchitecture. Mitochondrial crista structure is linked tightly to mitochondrial function. Non-foveal cone photoreceptors of primates contain considerably more inner segment mitochondria and have higher oxidative enzyme activity than do rods. In addition, it is suggested that light-adapted cones have a higher aerobic ATP demand than rods. Therefore, we investigated the oxidative metabolism and three-dimensional membrane architecture of mouse rod and cone inner segment mitochondria. Our goals were to determine, in light-adapted mouse retinas, the: 1) number of mitochondria and oxidative enzyme activity in rod inner segment (RIS) and cone inner segment (CIS), 2) photoreceptor oxygen consumption (QOPR) and compare it to that in dark-adapted photoreceptors, 3) dimensions and connectivity of RIS and CIS mitochondrial cristae and contact sites, and 4) structural motifs of RIS and CIS cristae.
期刊论文(0)
专著(0)
科研奖励(0)
会议论文
Structural Analyses Core
  • 批准号:
    10496283
  • 项目类别:
  • 资助金额:
    $33.1万
  • 财政年份:
    2023
  • 负责人:
    GUY A PERKINS
  • 依托单位:
INHIBITION OF PROTEIN IMPORT INTO MITOCHONDRIA
INHIBITION OF PROTEIN IMPORT INTO MITOCHONDRIA
IN VIVO APOPTOSIS & MITOCHONDRIA
海外基金