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Lurcher purkinje cells express glutamic acid decarboxylase and calbindin mRNAs
Author(s) -
Wuenschell C. W.,
Messer A.,
Tobin A. J.
Publication year - 1990
Publication title -
journal of neuroscience research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.72
H-Index - 160
eISSN - 1097-4547
pISSN - 0360-4012
DOI - 10.1002/jnr.490270110
Subject(s) - calbindin , purkinje cell , glutamate decarboxylase , in situ hybridization , biology , microbiology and biotechnology , cerebellum , degeneration (medical) , glutamate receptor , neuroscience , gene expression , gene , immunohistochemistry , pathology , genetics , biochemistry , immunology , enzyme , medicine , receptor
Purkinje neurons in immature Lurcher (Lc/ +) mice are destined to die as a result of a defect intrinsic to the dying cells. We have used in situ hybridization to determine whether the Lc allele interferes with the normal program of gene expression in the doomed Purkinje cells. In P21 mice, degeneration of Purkinje cells is well underway, but the surviving Purkinje cells continue to express the mRNAs for both glutamate decarboxylase and calbindin D 28k , two proteins whose expression is characteristic of normal Purkinje neurons. We conclude that the Lc allele probably does not interfere with the developmental program but acts to cause cell death in already differentiated Purkinje neurons.