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      Possible involvement of the cerebellum in motor-function impairment in progranulin-deficient mice.

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          Abstract

          Progranulin (PGRN) is a multifunctional growth factor involved in many physiological and pathological processes in the brain such as sexual differentiation, neurogenesis, neuroinflammation, and neurodegeneration. Previously, we showed that PGRN was expressed broadly in the brain and the Purkinje cells in the cerebellum were one of the regions with the highest expression level of PGRN. Thus, in the present study, we investigated the possible roles of PGRN in the cerebellum by comparing wild-type (WT) and PGRN-deficient (KO) mice with immunohistochemical staining for calbindin, a marker of Purkinje cells. The results showed that the density of Purkinje cell dendrites in the molecular layer of the cerebellum was significantly higher in KO mice than in WT mice, although the number of cell bodies was comparable between the genotypes. Subsequently, as the cerebellum is the center of the motor function, we performed a rotarod test and found that KO mice remained on the rotating rod for significantly shorter periods than WT mice. However, KO and WT mice did not differ significantly with respect to the diameter of myofibers in a skeletal muscle. These results suggest that PGRN is involved in the development and/or maturation of neuronal networks comprising Purkinje cells in the cerebellum, which may be a prerequisite to normal motor function.

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          Author and article information

          Journal
          Neuroreport
          Neuroreport
          Ovid Technologies (Wolters Kluwer Health)
          1473-558X
          0959-4965
          Sep 30 2015
          : 26
          : 14
          Affiliations
          [1 ] Department of Veterinary Physiology, Graduate School of Agricultural and Life Sciences, The University of Tokyo, Tokyo, Japan.
          Article
          00001756-201510010-00013
          10.1097/WNR.0000000000000442
          26302163
          a5a138f3-782a-4f76-bfa3-fdc73d42a930
          History

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