Ootsuka Youichirou, Nalivaiko Eugene, Blessing William W
Department of Human Physiology, School of Medicine, Flinders University, Bedford Park, South Australia 5042, Australia.
Brain Res. 2004 Jul 16;1014(1-2):34-44. doi: 10.1016/j.brainres.2004.03.058.
We determined whether spinal 5-hydroxytryptamine 2A (5-HT2A) receptors contribute to resting cutaneous sympathetic vasomotor activity, and to increases in activity elicited by electrical stimulation of the medullary raphe/parapyramidal region, and whether these receptors are involved in the cutaneous vasoconstricting action of systemically administered MDMA (3,4-methylenedioxymethamphetamine, "Ecstasy") and its reversal by clozapine. Experiments were conducted in urethane-anesthetized rabbits and rats. Administration of the 5-HT2A antagonist, trans-4-((3Z)3-[(2-Dimethylaminoethyl)oxyimino]-3-(2-fluorophenyl)propen-1-yl)-phenol, hemifumarate (SR 46349B, 0.1 mg/kg, i.v.) inhibited resting ear pinna sympathetic vasomotor nerve discharge and reduced the extent to which raphe/parapyramidal electrical stimulation caused ear pinna (rabbit) and tail (rat) artery blood flow to fall. Clozapine (0.125-0.5 mg/kg, i.v.) also reduced the fall in ear pinna blood flow elicited by raphe/parapyramidal stimulation. In rabbits, after inactivation of raphe/parapyramidal function by local microinjection of muscimol (1 nmol in 100 nl), the 5-HT2A agonist R(-)-1-(2,5-dimethoxy-4-iodophenyl)-2-aminopropane hydrochloride (DOI, 50 microg/kg, i.v.) increased ear pinna sympathetic nerve activity from 3+/-2% to 129+/-5% of pre-muscimol levels (P<0.01, n=6), and this increase was abolished by section of the ipsilateral cervical sympathetic nerve trunk. MDMA (2 mg/kg, i.v.) after muscimol decreased ear pinna blood flow from 33+/-10 to 2+/-1 cm/s (P<0.01, n=5) and increased ear pinna sympathetic nerve activity from 8+/-4% to 120+/-41% of pre-muscimol levels (P<0.01, n=6). The MDMA-elicited increase in nerve activity was abolished by SR 46349B. Data suggest that spinal 5-HT2A receptors contribute to sympathetically induced cutaneous vasoconstriction regulated by raphe/parapyramidal neurons in the brainstem, and that these receptors contribute to the cutaneous vasoconstricting action of MDMA and its reversal by clozapine.
我们研究了脊髓5-羟色胺2A(5-HT2A)受体是否参与静息时皮肤交感神经血管舒缩活动以及延髓中缝/锥体旁区域电刺激所引发的活动增加,还研究了这些受体是否参与全身给予摇头丸(3,4-亚甲基二氧基甲基苯丙胺,“摇头丸”)的皮肤血管收缩作用及其被氯氮平逆转的过程。实验在氨基甲酸乙酯麻醉的兔和大鼠身上进行。给予5-HT2A拮抗剂反式-4-((3Z)3-[(2-二甲基氨基乙基)氧基亚氨基]-3-(2-氟苯基)丙烯-1-基)-苯酚,半富马酸盐(SR 46349B,0.1毫克/千克,静脉注射)可抑制静息时耳廓交感神经血管舒缩神经放电,并减少中缝/锥体旁电刺激导致的耳廓(兔)和尾部(大鼠)动脉血流下降的程度。氯氮平(0.125 - 0.5毫克/千克,静脉注射)也可减少中缝/锥体旁刺激引起的耳廓血流下降。在兔身上,通过局部微量注射蝇蕈醇(100纳升中含1纳摩尔)使中缝/锥体旁功能失活后,5-HT2A激动剂R(-)-1-(2,5-二甲氧基-4-碘苯基)-2-氨基丙烷盐酸盐(DOI,50微克/千克,静脉注射)使耳廓交感神经活动从蝇蕈醇处理前水平的3±2%增加至129±5%(P<0.01,n = 6),且这种增加在切断同侧颈交感神经干后被消除。蝇蕈醇处理后给予摇头丸(2毫克/千克,静脉注射)使耳廓血流从33±10降至2±1厘米/秒(P<0.01,n = 5),并使耳廓交感神经活动从蝇蕈醇处理前水平的8±4%增加至120±41%(P<0.01,n = 6)。摇头丸引起的神经活动增加被SR 46349B消除。数据表明,脊髓5-HT2A受体参与脑干中缝/锥体旁神经元调节的交感神经诱导的皮肤血管收缩,且这些受体参与摇头丸的皮肤血管收缩作用及其被氯氮平逆转的过程。