Microtubule affinity‐regulating kinase 1 (MARK1) is activated by electroconvulsive shock in the rat hippocampus

• Published in: Journal of neurochemistry 2005-12, Vol.95 (6), p.1608-1618
• Main Authors: Jeon, Songhee, Kim, Yong‐Sik, Park, Joobae, Bae, Chang‐Dae
• Format: Article
• Language: English
• Subjects: Amino Acid Sequence; Animals; Biochemistry; Biological and medical sciences; Brain-Derived Neurotrophic Factor - pharmacology; brain‐derived neurotrophic factor; Cell Line, Tumor; Cell structures and functions; Central nervous system; Central neurotransmission. Neuromudulation. Pathways and receptors; Cytoskeleton, cytoplasm. Intracellular movements; depolarization; electroconvulsive shock; Electroconvulsive therapy; Electrophoresis, Polyacrylamide Gel; Electroshock; Fundamental and applied biological sciences. Psychology; Hippocampus - physiology; Immunoblotting; Male; microtubule affinity‐regulated kinase 1; Molecular and cellular biology; Molecular Sequence Data; Neuronal Plasticity - drug effects; Neurosciences; Phosphorylation; Potassium Chloride - pharmacology; Protein-Serine-Threonine Kinases - metabolism; Rats; Rats, Sprague-Dawley; Rodents; Tau; tau Proteins - metabolism; Vertebrates: nervous system and sense organs
• ISSN: 0022-3042; 1471-4159
• DOI: 10.1111/j.1471-4159.2005.03505.x

Electroconvulsive shock (ECS) induces phosphorylation and dephosphorylation of many signaling molecules in the rat brain. While studying phosphorylated proteins in the rat brain after ECS, we observed a 100‐kDa protein that cross‐reacted with anti‐phospho‐p70 S6 kinase antibody, which was subsequently purified and identified as microtubule affinity‐regulating kinase 1 (MARK1). Purified MARK1 was phosphorylated at the Ser and Thr residues. MARK1 activation and subsequent Tau phosphorylation in the hippocampus after ECS was confirmed by an in‐gel kinase assay using tau protein as a substrate. MARK1 was maximally activated between 2 and 5 min after ECS, and Tau phosphorylation at Ser262 was also increased at 2 min and lasted to 1 h after ECS. Taken together, we concluded that ECS activated MARK1 and subsequently phosphorylated Tau at Ser262. Both MARK1 activity and Tau phosphorylation were increased in the rat hippocampus after chronic ECS where axonal remodeling was apparent. In order to investigate the physiologic stimuli which are involved in the activation of MARK1, SH‐SY 5Y cells were treated with brain‐derived neurotrophic factor or 60 mm KCl. Both stimuli were capable of inducing MARK activation.