Oligodendrocytes are generated from oligodendroglial progenitor cells (OPCs) which proliferate in the subventricular zone and migrate to formative white matter regions, where they further proliferate, differentiate, and form myelin sheaths around axons. In addition, mutations in K V7.4 are associated with progressive hearing loss –. Mutations in either K V7.2 or K V7.3 lead to benign familial neonatal seizures as do mutations in K V7.5. Their mutations have been associated with human neurological pathologies including auditory diseases. Inhibition of channel activity, by either a blocking drug such as linopirdine (DuP 996) or 10, 10-bis(4-pyridinyl- methyl)-9(10 H)-anthracenone (XE991), or expression of a dominant-negative K V7.2 construct, strongly enhances repetitive firing and even effects postnatal brain development. Recent evidences suggest that K V7 channels have profound effects on neuronal excitability –. In most neurons native K V7 channels are composed of K V7.2 and K V7.3 subunits or sometimes of homomeric K V7.2 subunits, , although probably with a contribution by K V7.5 subunits in some neurons K V7.4 subunits are predominantly expressed in the auditory and vestibular systems, but also probably contribute to K V7 channels in central dopaminergic neurons.
So far, homomeric compositions are shown for K V7.2-5 subunits heteromeric compositions are represented by K V7.2+3, K V7.3+4 and K V7.3+5 channels. In CNS, K V7 channels form through homo- or heteromeric assembly of K V7.2 to K V7.5 subunits.
There they form subunits of voltage-gated K + channel originally termed the ‘M-channel’ and the current called M current, which has been demonstrated to assist in stabilizing the membrane potential in the presence of depolarizing currents and contributing to the resting potential of neurons.
The KCNQ gene family encodes five voltage-gated delayed rectifier K + channels K V7.1-5, and four of these K V7.2-5 are expressed in the nervous system.
0 kommentar(er)
