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J Physiol Volume 586, Number 7, 1823-1832, April 1, 2008 DOI: 10.1113/jphysiol.2007.149450
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SYMPOSIUM REPORT

Kv7 channels: interaction with dopaminergic and serotonergic neurotransmission in the CNS

 Henrik H. Hansen1, Olivier Waroux2, Vincent Seutin2, Thomas J. Jentsch3, Susana Aznar4 and Jens D. Mikkelsen1,5

1 Department of Translational Neurobiology, NeuroSearch A/S, Ballerup, Denmark
2 Department of Pharmacology and Research Center for Cellular and Molecular Neurobiology, University of Liege, Belgium
3 Leibniz-Institut für Molekulare Pharmakologie (FMP) and Max Delbrück Centrum für Molekulare Medizin (MDC), Berlin, Germany
4 Neurobiology Research Unit and Center for Integrated Molecular Brain Imaging, Copenhagen University Hospital, Copenhagen, Denmark
5 Department of Life Sciences, Aalborg University, Aalborg, Denmark

Neuronal Kv7 channels (also termed KCNQ channels) are the molecular correlate of the M-current. The Kv7 channels activate at rather negative membrane potentials (≤ 60 mV), thereby ‘fine-tuning’ the resting membrane potential. The Kv7 channels are widely expressed in the brain with the Kv7.2, Kv7.3 and Kv7.5 channels being the most abundant. The Kv7.4 subunit has the most restricted brain regional expression being present in discrete nuclei of brainstem only. Kv7 channels are expressed at different subcellular locations, being on both somatodendritic, axonal and terminal sites. This complex subcellular distribution of Kv7 channels enables them to participate in both pre- and postsynaptic modulation of basal and stimulated excitatory neurotransmission. Activation of neuronal Kv7 channels limits repetitive firing thereby potentially limiting the generation of long bursts, with subsequent inhibition of monoaminergic neurotransmitter release. In this review, we focus on the influence of Kv7 channels on dopaminergic and serotonergic neurotransmission. The data suggest a novel action of Kv7 channel openers which could translate into having therapeutic value in the treatment of disease states characterized by overactivity of dopaminergic (e.g. schizophrenia and drug abuse) and serotonergic neurotransmission (e.g. anxiety).

(Received 6 December 2007; accepted after revision 2 January 2008; first published online 10 January 2008)
Corresponding author H. H. Hansen: Department of Translational Neurobiology, NeuroSearch A/S, Pederstrupvej 93, DK-2750 Ballerup, Denmark.  Email: heh{at}neurosearch.dk

This report was presented at a symposium on Kv7 (KCNQ) potassium channels that are mutated in human diseases, held at a joint meeting of The Slovak Physiological Society, The Physiological Society and The Federation of European Physiological Societies in Bratislava, Slovakia on 14 September 2007. It was commissioned by the Editorial Board and reflects the views of the authors.




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Kv7 (KCNQ) potassium channels that are mutated in human diseases
J. Physiol., April 1, 2008; 586(7): 1781 - 1783.
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