Ji-Eun Kim1, Sung-Eun Kwak, Tae-Cheon Kang. 1. Department of Anatomy and Neurobiology and Institute of Epilepsy Research, College of Medicine, Hallym University, Chunchon, South Korea.
Abstract
PURPOSE: To identify the modulation of Tandem of P-domains in a weak inwardly rectifying K(+) channel (TWIK)-related acid-sensitive K(+) (TASK)-2 channel expressions in epilepsy, we conducted a comparative analysis of TASK-2 channel immunoreactivity in the hippocampus of a pilocarpine-induced rat epilepsy model. METHODS: We performed and immunohistochemical study for TASK-2 and double immunofluorescent staining for TASK-2 and glial fibrillary acidic protein (GFAP) in the rat hippocampus of pilocarpine-induced epilepsy models. RESULTS: In control animals, TASK-2 immunoreactivity was strongly detected in CA1-3 pyramidal layers and dentate granule cell layer. After status epilepticus (SE), TASK-2 immunoreactivity was increased in dentate granule cell layer and CA3 pyramidal cell layer, whereas its immunoreactivity was reduced in CA1 pyramidal cell layer. In addition, TASK-2 immunoreactivity is gradually increased in perivascular regions following SE. Double immunofluorescent study revealed that the enhancement of TASK-2 immunoreactivity in perivascular regions is caused by increase in the number of TASK-2 immunoreactive endfeet of perivascular astrocytes. DISCUSSION: Our findings suggest that elevated TASK-2 immunoreactivity in neurons may contribute to rapid adaptive responses (presumably for extracellular alkalinization), which result in hyperpolarization and regulate seizure activity. In contrast, upregulated TASK-2 immunoreactivity in perivascular regions may be involved in abnormalities of blood flow regulation or brain-blood barrier impairment. These changes may contribute to acquisition of the properties of the epileptic hippocampus.
PURPOSE: To identify the modulation of Tandem of P-domains in a weak inwardly rectifying K(+) channel (TWIK)-related acid-sensitive K(+) (TASK)-2 channel expressions in epilepsy, we conducted a comparative analysis of TASK-2 channel immunoreactivity in the hippocampus of a pilocarpine-induced ratepilepsy model. METHODS: We performed and immunohistochemical study for TASK-2 and double immunofluorescent staining for TASK-2 and glial fibrillary acidic protein (GFAP) in the rat hippocampus of pilocarpine-induced epilepsy models. RESULTS: In control animals, TASK-2 immunoreactivity was strongly detected in CA1-3 pyramidal layers and dentate granule cell layer. After status epilepticus (SE), TASK-2 immunoreactivity was increased in dentate granule cell layer and CA3 pyramidal cell layer, whereas its immunoreactivity was reduced in CA1 pyramidal cell layer. In addition, TASK-2 immunoreactivity is gradually increased in perivascular regions following SE. Double immunofluorescent study revealed that the enhancement of TASK-2 immunoreactivity in perivascular regions is caused by increase in the number of TASK-2 immunoreactive endfeet of perivascular astrocytes. DISCUSSION: Our findings suggest that elevated TASK-2 immunoreactivity in neurons may contribute to rapid adaptive responses (presumably for extracellular alkalinization), which result in hyperpolarization and regulate seizure activity. In contrast, upregulated TASK-2 immunoreactivity in perivascular regions may be involved in abnormalities of blood flow regulation or brain-blood barrier impairment. These changes may contribute to acquisition of the properties of the epileptic hippocampus.
Authors: Christina C Young; Michael Stegen; René Bernard; Martin Müller; Josef Bischofberger; Rüdiger W Veh; Carola A Haas; Jakob Wolfart Journal: J Physiol Date: 2009-06-29 Impact factor: 5.182
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