Research Report Expression of BK Ca channels and the modulatory β-subunits in the rat and porcine trigeminal ganglion Helle Wulf-Johansson a, ⁎ , Anders Hay-Schmidt b , Asser Nyander Poulsen c , Dan Arne Klaerke c , Jes Olesen a , Inger Jansen-Olesen a a Department of Neurology and Danish Headache Center, Glostrup Research Institute, Glostrup Hospital, Faculty of Health Sciences, University of Copenhagen, 2600 Glostrup, Denmark b Department of Neuroscience and Pharmacology, Faculty of Health Sciences, University of Copenhagen, 2100 Copenhagen, Denmark c Department of Physiology and Biochemistry, IBHV, Faculty of Life Sciences, University of Copenhagen, 1870 Frederiksberg, Denmark ARTICLE INFO ABSTRACT Article history: Accepted 14 July 2009 Available online 23 July 2009 Large conductance calcium-activated potassium (BK Ca ) channels contribute to electrical impulses, proper signal transmission of information and regulation of neurotransmitter release. Migraine has been proposed to be a trigeminovascular disease involving the sensory trigeminal pathways and the cerebral arteries. We hypothesize that BK Ca channel α- and β- subunits are present in the rat and porcine trigeminal ganglion (TG) thus enabling a role in migraine. BK Ca channel mRNA was detected using reverse transcription polymerase chain reaction (RT-PCR) and in situ hybridization. BK Ca channel protein was visualized by western blotting and histochemistry. The presence of the modulatory β1–β4 subunit mRNAs was investigated using RT-PCR. β1-, β2- and β4-subunit mRNAs were expressed in rat TG whereas β2- and β4-subunits were detected in porcine TG. Western blotting revealed β2- and β4-subunit proteins in rat and porcine TG. The present study showed BK Ca channel expression in rat and porcine TG. The main modulatory β-subunits detected in TG of both species were β2- and β4-subunits. © 2009 Elsevier B.V. All rights reserved. Keywords: BK Ca channel Trigeminal ganglion Calcitonin gene-related peptide In situ hybridization Histochemistry Pain 1. Introduction Migraine pain is thought to arise from the trigeminovascular pathway (Goadsby et al., 2009; Ray and Wolff, 1940). The cell bodies of the trigeminal nerve are located in the trigeminal ganglion (TG) in close association with satellite glial cells. The trigeminal neurons have a pseudo-unipolar morphology dividing the axon into a peripheral and central branch. The peripheral sensory fibres innervate the large cerebral and meningeal blood vessels (O'Connor and van der Kooy, 1986) whereas the central fibres project to the trigeminal nucleus caudalis (TNC) in the brain stem, which transmits nociceptive information to higher brain centres and sensory cortex (Lazarov, 2002). Stimulation of the TG results in cerebral vaso- dilation (Goadsby et al., 1997) as a result of neuropeptide release (calcitonin gene-related peptide (CGRP), substance P and neurokinin A) from perivascular sensory nerve endings (Edvinsson et al., 1988; Goadsby et al., 1988; Liu-Chen et al., BRAIN RESEARCH 1292 (2009) 1 – 13 ⁎ Corresponding author. Department of Neurology, Danish Headache Center, Glostrup Research Institute, Glostrup Hospital, Nordre Ringvej 69, 2600 Glostrup, Denmark. Fax: +45 43 23 3983. E-mail address: helwul02@glo.regionh.dk (H. Wulf-Johansson). Abbreviations: BK Ca large conductance calcium-activated potassium channelsCGRPcalcitonin gene-related peptidePBSphosphate buffered salineRT-PCRreverse transcription polymerase chain reaction 0006-8993/$ – see front matter © 2009 Elsevier B.V. All rights reserved. doi:10.1016/j.brainres.2009.07.047 available at www.sciencedirect.com www.elsevier.com/locate/brainres