Xu X J, Wiesenfeld-Hallin Z
Department of Medical Laboratory Sciences and Technology, Huddinge University Hospital, Karolinska Institute, Sweden.
Eur J Pharmacol. 1995 Jan 16;272(2-3):219-22. doi: 10.1016/0014-2999(94)00646-o.
We have studied the effects of alpha-trinositol (D-myo-inositol-1,2,6-trisphosphate, PP56), a putative antagonist of neuropeptide Y receptors, on the nociceptive flexor reflex in decerebrate, spinalized rats after intrathecal and intravenous administration. Intrathecal alpha-trinositol caused strong and prolonged facilitation of the flexor reflex, which was usually associated with an increase in spontaneous motoneuron activity. The reflex depressive effect of intrathecal neuropeptide Y was neither blocked nor reversed by alpha-trinositol. Intravenous alpha-trinositol at low doses had no effect on the flexor reflex and at high dose, reflex facilitation was sometimes observed. It is concluded that alpha-trinositol acts as a spinal excitant and is not an antagonist of the neuropeptide Y receptor in the rat spinal cord.
我们研究了α-三磷酸肌醇（D-肌醇-1,2,6-三磷酸，PP56），一种假定的神经肽Y受体拮抗剂，在鞘内和静脉注射后对去大脑、脊髓横断大鼠伤害性屈肌反射的影响。鞘内注射α-三磷酸肌醇可引起屈肌反射强烈且持久的易化，这通常与自发运动神经元活动增加有关。鞘内注射神经肽Y的反射抑制作用既未被α-三磷酸肌醇阻断也未被其逆转。低剂量静脉注射α-三磷酸肌醇对屈肌反射无影响，高剂量时有时可观察到反射易化。结论是α-三磷酸肌醇在大鼠脊髓中起脊髓兴奋作用，而非神经肽Y受体的拮抗剂。
