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PICK1 expression in reactive astrocytes within the spinal cord of amyotrophic lateral sclerosis (ALS) rats

肌萎缩侧索硬化 兴奋毒性 脊髓 谷氨酸受体 腰脊髓 神经科学 生物 胶质纤维酸性蛋白 中枢神经系统 病理 免疫组织化学 医学 受体 免疫学 生物化学 疾病
作者
M. Focant,Stéphanie Goursaud,Cédric Boucherie,Amélie Dumont,Emmanuel Hermans
出处
期刊:Neuropathology and Applied Neurobiology [Wiley]
卷期号:39 (3): 231-242 被引量:8
标识
DOI:10.1111/j.1365-2990.2012.01282.x
摘要

M. C. Focant, S. Goursaud, C. Boucherie, A. O. Dumont and E. Hermans (2013) Neuropathology and Applied Neurobiology 39, 231–242 PICK1 expression in reactive astrocytes within the spinal cord of amyotrophic lateral sclerosis (ALS) rats Aims: The protein interacting with C kinase 1 (PICK1), a PDZ domain‐containing protein mainly expressed in the central nervous system, interacts with the glutamate receptor subunit GluR2, with the glutamate transporter GLT‐1b and with the enzyme serine racemase. These three proteins appear as key actors in the glutamate‐mediated excitotoxicity associated with amyotrophic lateral sclerosis (ALS), in both patients and animal models of the disease. In this study, we examined the expression of PICK1 in the spinal cord of transgenic rats expressing a mutated form of the human superoxide dismutase 1 (hSOD1 G93A ) during the progression of the disease. Methods: Expression of PICK1 was examined by real‐time qPCR at presymptomatic and symptomatic stages as well as at end‐stage. The expression of PICK1 in the different cell types of the spinal cord was examined by immunohistochemistry. Results: The overall expression of PICK1 is not modified in cervical and lumbar spinal cord of transgenic (hSOD1 G93A ) rats during the progression of the disease. Nonetheless, immunohistochemical studies of lumbar ventral horns revealed a shift of PICK1 expression from motor neurones in healthy rats to activated astrocytes in end‐stage hSOD1 G93A animals. Conclusions: Considering the documented influence of PICK1 expression on d ‐serine release and glutamate transport in astrocytes, these findings point to a potential implication of PICK1 in the progression of ALS.
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