Abstract
BackgroundKV7/KCNQ channels are widely expressed in neurons and they have multiple important functions, including control of excitability, spike afterpotentials, adaptation, and theta resonance. Mutations in KCNQ genes have been demonstrated to associate with human neurological pathologies. However, little is known about whether KV7/KCNQ channels are expressed in oligodendrocyte lineage cells (OLCs) and what their functions in OLCs.Methods and FindingsIn this study, we characterized KV7/KCNQ channels expression in rat primary cultured OLCs by RT-PCR, immunostaining and electrophysiology. KCNQ2-5 mRNAs existed in all three developmental stages of rat primary cultured OLCs. KV7/KCNQ proteins were also detected in oligodendrocyte progenitor cells (OPCs, early developmental stages of OLCs) of rat primary cultures and cortex slices. Voltage-clamp recording revealed that the IM antagonist XE991 significantly reduced KV7/KCNQ channel current (IK(Q)) in OPCs but not in differentiated oligodendrocytes. In addition, inhibition of KV7/KCNQ channels promoted OPCs motility in vitro.ConclusionsThese findings showed that KV7/KCNQ channels were functionally expressed in rat primary cultured OLCs and might play an important role in OPCs functioning in physiological or pathological conditions.
Highlights
The KCNQ gene family encodes five voltage-gated delayed rectifier K+ channels KV7.1-5, and four of these KV7.2-5 are expressed in the nervous system [1,2]
These findings showed that KV7/KCNQ channels were functionally expressed in rat primary cultured oligodendrocyte lineage cells (OLCs) and might play an important role in oligodendroglial progenitor cells (OPCs) functioning in physiological or pathological conditions
The mRNAs of KV7.2–5/ KCNQ2-5 were detected in rat primary cultured OLCs
Summary
The KCNQ gene family encodes five voltage-gated delayed rectifier K+ channels KV7.1-5, and four of these KV7.2-5 are expressed in the nervous system [1,2]. Inhibition of channel activity, by either a blocking drug such as linopirdine (DuP 996) [16] or 10, 10-bis(4pyridinyl- methyl)-9(10 H)-anthracenone (XE991), or expression of a dominant-negative KV7.2 construct, strongly enhances repetitive firing and even effects postnatal brain development [17]. Their mutations have been associated with human neurological pathologies including auditory diseases [1,2]. Little is known about whether KV7/KCNQ channels are expressed in oligodendrocyte lineage cells (OLCs) and what their functions in OLCs
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