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垂体β-内啡肽与刺激下丘脑弓状核镇痛的关系

Relationship Between Pituitary β-Endorphin and Analgesia Produced by Stimulation of Hypothalamic Arcuate Nucleus

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【摘要】 电刺激大鼠下丘脑弓状核可产生明显镇痛效应,并使脑内β-内啡肽含量升高,该镇痛效应可被腹腔内注射地塞米松所阻断。摘除垂体亦可使刺激弓状核的镇痛效应基本消失,这时,脑内β-内啡肽含量也不明显升高。结果揭示,刺激弓状核有可能激活垂体β-内啡肽的释放,循垂体门脉系统逆流入脑,从而参与镇痛作用的发挥。这可能是刺激弓状核产生镇痛效应的机制之一.

【Abstract】 Electrical stimulation of rat hypothalamic arcuate nucleus(ARC)could produce a marked analgesia with concomitant increase of β-endorphin(β-END)content in the brain.This analgesia could be blocked by intraperitoneal injection of dexamethasone.After hypophysectomy,ARC stimulation could neither produce an analgesia nor increase β-END content in the brain.These results suggest that pituitary β-END might be acti- vated and released by ARC stimulation and flow retrogradely into the brain via portal ves- sel system to participate in the analgesia produced by ARC stimulation.This might be one of the mechanisms underlying the analgesia produced by ARC stimulation.

【基金】 国家自然科学基金课题
  • 【文献出处】 苏州医学院学报 ,Suzhou University Journal of Medical Science , 编辑部邮箱 ,1989年04期
  • 【被引频次】4
  • 【下载频次】53
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