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Phosphorylation and Activation of Mitogen-Activated Protein Kinase by Kainic Acid-Induced Seizure in Rat Hippocampus

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Abstract

Injection of kainic acid into rat induced a limbic seizure and increased the activities of two protein kinases with Mrs of 42 kDa and 44 kDa in the hippocampus. These two protein kinases were identified as MAP kinases by an anti-MAP kinase antibody. These MAP kinases were phosphorylated at least at a tyrosine residue. The time course of the MAP kinase activation was roughly parallel with that of the seizure. These results indicate that the kainic acid-induced seizure induces MAP kinase activation in rat hippocampus.

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    A number of studies using cultured neurons have shown that ERK1/2 is activated in response to excitatory glutamatergic stimulation and following Ca2+-influx into neurons (Bading and Greenberg, 1991; Fiore et al., 1993; Kurino et al., 1995; Murphy et al., 1994). Robust ERK1/2 activation has also been observed in various types of seizure models, implicating a close relationship between neuronal excitation and ERK1/2 activation in vivo (Baraban et al., 1993; Gass et al., 1993; Kim et al., 1994; Murray et al., 1998; Merlo et al., 2004; Jeon et al., 2000; Lugo et al., 2008; de Lemos et al., 2010; Yamagata et al., 2002, 2013). Elucidating signaling cascades that involve ERK1/2 has been a focus of attention, especially in the context of synaptic plasticity and learning and memory, and a number of direct targets of ERK1/2 have been documented (Sweatt, 2004; Thomas and Huganir, 2004).

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