Potassium Channels of Glial Cells: Distribution and Function

Horio, Yoshiyuki

doi:10.1254/jjp.87.1

Cited by 33 publications

(19 citation statements)

References 30 publications

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“…We observed co-immunoprecipitation of Kir5.1 with PSD-95 in the optic nerve and a high degree of Kir5.1 immunolabelling in optic nerve glia was not associated with Kir4.1, raising the possibility they may express functional homomeric Kir5.1 channels. However, Kir5.1 may also form heteromers with other Kir subtypes, including Kir2.1 (Derst et al 2001; Pessia et al 2001), which is expressed by astrocytes (Horio 2001; Howe et al 2008; Kang et al 2008), and also clusters with PSD-95 (Fomina et al 2011; Nehring et al 2000; Leonoudakis et al 2001; Pegan et al 2007). Our results identified that Kir5.1 immunolabeling was mostly concentrated within the cell cytoplasm, tenfold greater than at the plasmalemma, indicating they provide a pool by which plasmallemal Kir4.1/Kir5.1 channels could be inserted into the cell membrane and provide dynamic regulation of the glial membrane potential in response to changes in the extracellular environment (Bolton and Butt 2006; Bolton et al 2006).…”

Section: Discussionmentioning

confidence: 99%

Expression of Kir4.1 and Kir5.1 inwardly rectifying potassium channels in oligodendrocytes, the myelinating cells of the CNS

et al. 2016

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The inwardly rectifying K+ channel subtype Kir5.1 is only functional as a heteromeric channel with Kir4.1. In the CNS, Kir4.1 is localised to astrocytes and is the molecular basis of their strongly negative membrane potential. Oligodendrocytes are the specialised myelinating glia of the CNS and their resting membrane potential provides the driving force for ion and water transport that is essential for myelination. However, little is known about the ion channel profile of mature myelinating oligodendrocytes. Here, we identify for the first time colocalization of Kir5.1 with Kir4.1 in oligodendrocytes in white matter. Immunolocalization with membrane-bound Na+/K+-ATPase and western blot of the plasma membrane fraction of the optic nerve, a typical CNS white matter tract containing axons and the oligodendrocytes that myelinate them, demonstrates that Kir4.1 and Kir5.1 are colocalized on oligodendrocyte cell membranes. Co-immunoprecipitation provides evidence that oligodendrocytes and astrocytes express a combination of homomeric Kir4.1 and heteromeric Kir4.1/Kir5.1 channels. Genetic knock-out and shRNA to ablate Kir4.1 indicates plasmalemmal expression of Kir5.1 in glia is largely dependent on Kir4.1 and the plasmalemmal anchoring protein PSD-95. The results demonstrate that, in addition to astrocytes, oligodendrocytes express both homomeric Kir4.1 and heteromeric Kir4.1/Kir5.1 channels. In astrocytes, these channels are essential to their key functions of K+ uptake and CO2/H+ chemosensation. We propose Kir4.1/Kir5.1 channels have equivalent functions in oligodendrocytes, maintaining myelin integrity in the face of large ionic shifts associated with action potential propagation along myelinated axons.

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Section: Discussionmentioning

confidence: 99%

Expression of Kir4.1 and Kir5.1 inwardly rectifying potassium channels in oligodendrocytes, the myelinating cells of the CNS

et al. 2016

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“…During RNAi, the K ϩ buffering capacity of SGCs (Haydon, 2001; Butt and Kalsi, 2006) would significantly decrease, with a consequent increase in extracellular K ϩ . It should also be noted that, although other K ϩ channels are present on both SGCs (Vit et al, 2006) and CNS glial cells (Horio, 2001), the best evidence indicate they cannot compensate for the silencing of Kir4.1 (Kucheryavykh et al, 2007).…”

Section: Discussionmentioning

confidence: 99%

Silencing the Kir4.1 Potassium Channel Subunit in Satellite Glial Cells of the Rat Trigeminal Ganglion Results in Pain-Like Behavior in the Absence of Nerve Injury

Vit¹,

Ohara²,

Bhargava³

et al. 2008

J. Neurosci.

175

157

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Growing evidence suggests that changes in the ion buffering capacity of glial cells can give rise to neuropathic pain. In the CNS, potassium ion (K ϩ ) buffering is dependent on the glia-specific inward rectifying K ϩ channel Kir4.1. We recently reported that the satellite glial cells that surround primary sensory neurons located in sensory ganglia of the peripheral nervous system also express Kir4.1, whereas the neurons do not. In the present study, we show that, in the rat trigeminal ganglion, the location of the primary sensory neurons for face sensation, specific silencing of Kir4.1 using RNA interference leads to spontaneous and evoked facial pain-like behavior in freely moving rats. We also show that Kir4.1 in the trigeminal ganglion is reduced after chronic constriction injury of the infraorbital nerve. These findings suggests that neuropathic pain can result from a change in expression of a single K ϩ channel in peripheral glial cells, raising the possibility of targeting Kir4.1 to treat pain in general and particularly neuropathic pain that occurs in the absence of nerve injury.

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“…The fluids of the inner ear, endolymph and perilymph, have at least two roles – to transduce the signal to the cochlear and vestibular hair cells, and to participate in the ionic exchanges between fluid and hair cells [106]. The endolymph is a potassium-rich extracellular fluid, whereas the perilymph has a composition closer to that of extracellular fluid [107]. It is well-known that vestibular functions can be altered by a number of peptide e.g arginine vasopressin, and steroid hormones [108-110], which act by changing composition, and maybe the volume, of the endolymph.…”

Section: Brain-central Nervous System Eye Ear-fluid Compartmentsmentioning

confidence: 99%

“…Of these it seems that AQP4 provides the principal route for water transport in astrocytes [113]. Glial cells are indispensable for regulating ionic homeostasis, particularly in aspirating the excess extracellular potassium which occurs after neural excitation [107]. It is of interest that in the specialized glial Muller cells of the eye, there is a close correlation between concentrations of the potassium channel, Kir4.1 and AQP4 levels [114], and retinal function is mildly impaired in mice lacking AQP4 [115].…”

Section: Brain-central Nervous System Eye Ear-fluid Compartmentsmentioning

confidence: 99%

Aquaporins in development – a review

Liu

Wintour

2005

Reprod Biol Endocrinol

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Water homeostasis during fetal development is of crucial physiologic importance. It depends upon maternal fetal fluid exchange at the placenta and fetal membranes, and some exchange between fetus and amniotic fluid can occur across the skin before full keratinization. Lungs only grow and develop normally with fluid secretion, and there is evidence that cerebral spinal fluid formation is important in normal brain development. The aquaporins are a growing family of molecular water channels, the ontogeny of which is starting to be explored. One question that is of particular importance is how well does the rodent (mouse, rat) fetus serve as a model for long-gestation mammals such as sheep and human? This is particularly important for organs such as the lung and the kidney, whose development before birth is very much less in rodents than in the long-gestation species.

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Potassium Channels of Glial Cells: Distribution and Function

Cited by 33 publications

References 30 publications

Expression of Kir4.1 and Kir5.1 inwardly rectifying potassium channels in oligodendrocytes, the myelinating cells of the CNS

Expression of Kir4.1 and Kir5.1 inwardly rectifying potassium channels in oligodendrocytes, the myelinating cells of the CNS

Silencing the Kir4.1 Potassium Channel Subunit in Satellite Glial Cells of the Rat Trigeminal Ganglion Results in Pain-Like Behavior in the Absence of Nerve Injury

Aquaporins in development – a review

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