【摘 要】
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Objective Hydrogen sulfide (H2S), an endogenous gaseotransmitter/modulator, is becoming appreciated that it may be involved in a wide variety of processes including inflammation and nociception.Howeve
【机 构】
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Department of Stomatology (Department of Oral and Maxillofacial Surgery), Affiliated Hospital of Nan
【出 处】
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中国神经科学学会第九届全国学术会议暨第五届会员代表大会
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Objective Hydrogen sulfide (H2S), an endogenous gaseotransmitter/modulator, is becoming appreciated that it may be involved in a wide variety of processes including inflammation and nociception.However, the role and mechanism for H2S in nociceptive processing in trigeminal ganglion (TG) neuron remains unknown.The present study is to explore the role of H2S on voltage-gated potassium channels and the distribution of endogenous H2S synthyzing enzyme CBS expression in TG neurons, Methods Whole cell patch clamp recordings were employed on acutely isolated TG neurons from adult male Sprague Dawley rats (6-8 week old).Immunofluorescence studies were carried out to determine whether CBS was co-expressed in Kvl.1 or Kvl.4-positive TG neurons.Results In rat TG, (77.0±6.6)% neurons were immunoreactive for CBS, (85.1±3.8)% for Kv1.1 and (97.8±1.1)% for Kv1.4.Double staining showed that all the CBS labeled cells were Kv1.1 and Kv1.4 positive, but only (92.2±6.1)% of Kv1.1 and (78.2±9.9)% of Kv1.4 positive cells contained CBS, respectively.Application of H2S donor NaH S (250 μM) led to a significant depolarization of resting membrane potential recorded from TG neurons (n=8, P<0.05).Application of NaHS also resulted in a dramatic reduction in rheobase (P<0.05), hyperpolarization of action potential threshold (P<0.05), and a significant increase in the number of action potentials evoked at 2X and 3X rheobase stimulation (P<0.05).Under voltage-clamp conditions, TG neurons exhibited transient A-type (IA) and sustained outward rectifier K+ currents (IK).Application of NaHS did suppress the IK density while did not change the IA density of TG neurons (n=6).Conclusion These data suggest that H2S generated by endogenously expressed CBS in TG neurons increases neuronal excitability, which is largely mediated by suppressing IK density, thus identifying for the first time a specific molecular mechanism underlying pain and sensitization in TG.
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