Activation of GABAB receptors potentiates inward rectifying potassium currents in satellite glial cells from rat trigeminal ganglia: In vivo patch-clamp analysis
| Autor: | Yoshihito Shimazu, Mamoru Takeda, Takuya Kanazawa, Masanori Nasu |
|---|---|
| Rok vydání: | 2015 |
| Předmět: |
Male
Agonist Baclofen Patch-Clamp Techniques medicine.drug_class Dose-Response Relationship Immunologic GABAB receptor Membrane Potentials GABA Antagonists Trigeminal ganglion chemistry.chemical_compound medicine Animals Patch clamp Potassium Channels Inwardly Rectifying Rats Wistar Receptor Membrane potential Chemistry General Neuroscience Hyperpolarization (biology) Immunohistochemistry Cell biology Microscopy Fluorescence Receptors GABA-B Trigeminal Ganglion nervous system Barium GABA-B Receptor Agonists Saclofen Neuroglia Neuroscience |
| Zdroj: | Neuroscience. 288:51-58 |
| ISSN: | 0306-4522 |
| DOI: | 10.1016/j.neuroscience.2014.12.024 |
| Popis: | 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 GABA B 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 GABA B 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 GABA B 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 GABA B 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. |
| Databáze: | OpenAIRE |
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