Upregulated TWIK‐related acid‐sensitive K+ channel‐2 in neurons and perivascular astrocytes in the hippocampus of experimental temporal lobe epilepsy

Abstract

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. 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. 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. 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.