Suppression of ATP-induced excitability in rat small-diameter trigeminal ganglion neurons by activation of GABAB receptor.
作者： Mamoru Takeda , Mizuho Ikeda , Masayuki Takahashi , Takuya Kanazawa , Masanori Nasu
DOI: 10.1016/J.BRAINRESBULL.2013.08.005
关键词:
摘要: Abstract The aim of the present study was to investigate whether a GABAB receptor agonist could modulate ATP-activated neuronal excitability nociceptive TRG neurons using perforated whole-cell patch-clamp and immunohistochemical techniques. Immunohistochemical analysis revealed that 86% P2X3 receptor-immunoreactive, small-diameter co-expressed receptor. Under voltage-clamp conditions (Vh = −60 mV), application ATP activated inward current in acutely isolated rat dose-dependent manner (10–50 μM) this be blocked by pyridoxal-phosphate-6-azophenyl-27,47-disulfonic acid (PPADS) (10 μM), selective P2 purinoreceptor antagonist. peak amplitude currents significantly inhibited after agonist, baclofen (10–50 μM), concentration-dependent reversible manner. baclofen-induced inhibition abolished co-application 3-amino-2 (4-chlorophenyl)-2hydroxypropysufonic acid) saclofen, antagonist (50 μM). current-clamp conditions, 20 μM depolarized membrane potential resulting increased mean action frequencies, these ATP-induced effects were antagonized saclofen. Together, results suggested activation inhibit through Thus, interaction between receptors cell bodies is therapeutic target for treatment trigeminal nociception.
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