☆ 4.6 Article

Loss of Purkinje cells in the PKCγ H101Y transgenic mouse

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS (2009)

Journal

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS

Volume 378, Issue 3, Pages 524-528

Publisher

ACADEMIC PRESS INC ELSEVIER SCIENCE

DOI: 10.1016/j.bbrc.2008.11.082

Keywords

Protein kinase C gamma; Spinocerebellar ataxia type 14; Purkinje cell; Gap junctions; Endoplasmic reticulum stress; Apoptosis

Categories

Biochemistry & Molecular Biology Biophysics

Funding

NIH01 EY013421
National Organization for Rare Disorders grant
[P20RR-017686]
[P20-RR-016475]

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Abstract

Spinocerebellar ataxia type 14 (SCA14) is an autosomal, dominant neurodegenerative disorder caused by mutations in PKC gamma. The objective of this study was to determine effects of PKC gamma H101Y SCAM mutation on Purkinje cells in the transgenic mouse. Results demonstrated that wild type PKC gamma-like Purkinje cell localization of HA-tagged PKCy H101Y mutant proteins, altered morphology and loss of Purkinje cells were observed in the PKCy H101Y SCA14 transgenic mouse at four weeks of age. Failure of stereotypical clasping responses in the hind limbs of transgenic mice was also observed. Further, PKC gamma H101Y SCA14 mutation caused lack of total cellular PKCy enzyme activity, loss of connexin 57 phosphorylation on serines, and activation of caspase-12 in the PKC gamma H101Y SCA14 transgenic mouse. Results clearly demonstrate a need for PI(Cy control of gap junctions for maintenance of Purkinje cells. This is the first transgenic mouse to our knowledge which models a human SCA14 mutation. (C) 2008 Elsevier Inc. All rights reserved.

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The effects of noise exposure on hippocampal cognition in C57BL/6 mice via transcriptomics

Zan Zhou, Wen-jun Jiang, Li Li, Jun-qiang Si

Summary: This study investigates the effect of noise exposure on cognitive function in mice and explores the underlying molecular mechanisms. The findings suggest that noise exposure leads to increased inflammation, increased phosphorylation of Tau protein, and decreased levels of postsynaptic density protein, resulting in cognitive impairment.

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS (2024)

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