【摘 要】
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Evidence has shown that hypoxic episodes elicit hypoglossal neuroplasticity which depends on elevated serotonin(5-HT),in contrast to the rationale of obstructive sleep apnea(OSA)that deficient seroton
【机 构】
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Department of Respiratory Medicine, Zhongshan Hospital affiliated to Fudan University,Shanghai, Chin
【出 处】
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中国医师协会中西医结合医师分会呼吸病专家委员会第二届学术研讨会
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Evidence has shown that hypoxic episodes elicit hypoglossal neuroplasticity which depends on elevated serotonin(5-HT),in contrast to the rationale of obstructive sleep apnea(OSA)that deficient serotonergic input to HMs fails to keep airway patency.Therefore,understanding of the 5-HT dynamic changes at hypoglossal nucleus(HN)during chronic intermittent hypoxia(CIH)will be essential to central pathogenic mechanism and pharmacological therapy of OSA.Moreover,the effect of CIH on BDNF-TrkB signaling proteins was quantified in an attempt to elucidate cellular cascades/synaptic mechanisms following 5-HT alteration.Male rats were randomly exposed to normal air(control),intermittent hypoxia of 3 weeks(IH3)and 5 weeks(IH5)groups.Through electrical stimulation of dorsal raphe nuclei(DRN),we conducted amperometric technique with carbon fiber electrode in vivo to measure the real time release of 5-HT at Ⅻ nucleus.5-HT2A receptors immunostaining measured by intensity and c-Fos quantified visually were both determined by immunohistochemistry.
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