| 15733086 |
Larkman PM, Perkins EM: A TASK-like pH- and amine-sensitive 'leak' K+ conductance regulates neonatal rat facial motoneuron excitability in vitro. Eur J Neurosci. 2005 Feb;21(3):679-91.
A 'leak' potassium (K+) conductance (gK (Leak)) modulated by amine neurotransmitters is a major determinant of neonatal rat facial motoneuron excitability. Although the molecular identity of gK (Leak) is unknown, TASK-1 and TASK-3 channel mRNA is found in facial motoneurons. External pH, across the physiological range (pH 6-8), and noradrenaline (NA) modulated a conductance that displayed a relatively linear current/voltage relationship and reversed at the K+ equilibrium potential, consistent with inhibition of gK (Leak). The pH-sensitive current (I (pH)), was maximal around pH 8, fully inhibited near pH 6 and was described by a modified Hill equation with a pK of 7.1. The NA-induced current (I (NA)) was occluded at pH 6 and enhanced at pH 7.7. The TASK-1 selective inhibitor anandamide (10 microM), its stable analogue methanandamide (10 microM), the TASK-3 selective inhibitor ruthenium red (10 microM) and Zn2+ (100-300 microM) all failed to alter facial motoneuron membrane current or block I (NA) or I (pH). Isoflurane, a volatile anaesthetic that enhances heteromeric TASK-1/TASK-3 currents, increased gK (Leak). Ba2+, Cs+ and Rb+ blocked I (NA) and I (pH) voltage-dependently with maximal block at hyperpolarized potentials. 4-Aminopyridine (4-AP, 4 mM) voltage-independently blocked I (NA) and I (pH). In summary, gK (Leak) displays some of the properties of a TASK-like conductance. The linearity of gK (Leak) and an independence of activation on external [K+] suggests against pH-sensitive inwardly rectifying K+ channels. Our results argue against principal contributions to gK (Leak) by homomeric TASK-1 or TASK-3 channels, while the potentiation by isoflurane supports a predominant role for heterodimeric TASK-1/TASK-3 channels. |
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