title: Activation of GABA(B) receptors potentiates inward rectifying potassium currents in satellite glial cells from rat trigeminal ganglia: in vivo patch-clamp analysis.
abstract: In a previous study, we demonstrated that inflammation suppressed inward rectifying K(+) (Kir) currents in satellite glial cells (SGCs) from the trigeminal ganglia (TRGs) and that this impairment of glial potassium homeostasis in the trigeminal ganglion (TRG) contributed to trigeminal pain. The aim of the present study was to investigate whether activation of GABAB receptors modulates the Kir current in SGCs using in vivo patch-clamp and immunohistochemical techniques. Immunohistochemically, we found that immunoreactivity for glial-specific Kir channel subunit Kir4.1 and the GABAB receptor was co-expressed in SGCs from the TRGs. In vivo whole-cell recordings were made using SGCs from the TRGs of urethane-anesthetized rats. Application of baclofen, a GABAB receptor agonist, significantly increased the mean peak amplitude of Kir currents in a concentration-dependent and reversible manner. Baclofen-induced potentiation of the Kir current was abolished by co-application of 3-amino-2-(4-chlorophenyl)-2-hydroxyprophylsulfonic acid (saclofen). In addition, baclofen significantly potentiated the density of the Ba(2+)-sensitive Kir current, and resulted in hyperpolarization of the mean membrane potential. These results suggest that activation of GABAB receptors potentiates the Kir current in SGCs and that GABA released from the TRG neuronal soma could contribute to buffering of extracellular K(+) concentrations following excitation of TRG neurons during the processing of sensory information, including the transmission of noxious stimuli.
authors.affiliation: Laboratory of Food and Physiological Sciences, Department of Life and Food Sciences, School of Life and Environmental Sciences, Azabu University, 1-17-71, Fuchinobe, Chuo-ku, Sagamihara, Kanagawa 252-5201, Japan. Electronic address: m-takeda@azabu-u.ac.jp.
authors.forename: M
authors.initials: M
authors.lastname: Takeda
authors.affiliation: Research Center for Odontology, School of Life Dentistry at Tokyo, Nippon Dental University, 1-9-20, Fujimi-cho, Chiyoda-ku, Tokyo 102-8159, Japan.
authors.forename: M
authors.initials: M
authors.lastname: Nasu
authors.affiliation: Department of Physiology, School of Life Dentistry at Tokyo, Nippon Dental University, 1-9-20, Fujimi-cho, Chiyoda-ku, Tokyo 102-8159, Japan.
authors.forename: T
authors.initials: T
authors.lastname: Kanazawa
authors.affiliation: Laboratory of Food and Physiological Sciences, Department of Life and Food Sciences, School of Life and Environmental Sciences, Azabu University, 1-17-71, Fuchinobe, Chuo-ku, Sagamihara, Kanagawa 252-5201, Japan.
authors.forename: Y
authors.initials: Y
authors.lastname: Shimazu
mesh_terms: D000818:Animals; D001418:Baclofen / Q000031:analogs & derivatives / Q000494:pharmacology; D001464:Barium / Q000378:metabolism; D004306:Dose-Response Relationship, Immunologic; D018756:GABA Antagonists / Q000494:pharmacology; D058786:GABA-B Receptor Agonists / Q000494:pharmacology; D007150:Immunohistochemistry; D008297:Male; D008564:Membrane Potentials / Q000187:drug effects / Q000502:physiology; D008856:Microscopy, Fluorescence; D009457:Neuroglia / Q000187:drug effects / Q000502:physiology*; D018408:Patch-Clamp Techniques / Q000379:methods; D024661:Potassium Channels, Inwardly Rectifying / Q000378:metabolism*; D017208:Rats, Wistar; D018080:Receptors, GABA-B / Q000378:metabolism*; D012668:Trigeminal Ganglion / Q000187:drug effects / Q000502:physiology*; D000098854:Kcnj10 Channel
chemical_list: D018756:GABA Antagonists; D058786:GABA-B Receptor Agonists; D000098854:Kcnj10 Channel; D024661:Potassium Channels, Inwardly Rectifying; D018080:Receptors, GABA-B; D001464:Barium; D001418:Baclofen; C080629:saclofen
keywords: GABA; GABA(B) receptor; glial potassium homeostasis; inward rectifying K current; satellite glial cells; trigeminal ganglion