THE ACTIONS OF 5-HT1 AGONISTS AND ANTAGONISTS ON NOCICEPTIVE PROCESSING IN THE RAT SPINAL-CORD - RESULTS FROM BEHAVIORAL AND ELECTROPHYSIOLOGICAL STUDIES

THE ACTIONS OF 5-HT1 AGONISTS AND ANTAGONISTS ON NOCICEPTIVE PROCESSING IN THE RAT SPINAL-CORD - RESULTS FROM BEHAVIORAL AND ELECTROPHYSIOLOGICAL STUDIES
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DOI:
10.1016/0006-8993(94)91184-3
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发表时间:
1994-10-24
期刊:
影响因子:
2.9
通讯作者:
BARASI, S
BARASI, S
中科院分区:
医学3区
文献类型:
--
作者:
ALI, Z;WU, G;BARASI, S

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我们已经开发出一种技术,使药物被显微注射在麻醉大鼠的鞘内,而单个单位的记录,从背角神经元。使用这种技术与轻麻醉大鼠引起的甩尾潜伏期(TFL)的记录一起,我们发现,特定的5-HT 1a激动剂8-OH DPAT(15,150,300 nmol)增加从单个背角神经元记录的伤害性反应,并降低TFL。非特异性5-HT 1b激动剂TFMPP(300 nmol)和一般5-HT 1激动剂5-CT(0.3、3.0、30 nmol)均降低伤害性反应,并且对TFL的作用不一致。鞘内应用5-HT(130,260 nmol)一般减少伤害性神经元反应和增加TFL。然而,在少数实验中,5-HT增加了伤害性反应,并表明这种作用与5-HT 1a受体的激活有关。5-HT 1b受体的活性具有抑制或降低反应性的作用。背角神经元对与5-HT 1a受体活性相关的伤害性刺激的反应性增加可能与感受野大小的增加、脊髓伤害性反射的促进或向特定脑干部位的吻侧传递的便利化有关。
We have developed a technique which allows drugs to be microinjected intrathecally in anaesthetised rats whilst single unit recordings are made from dorsal horn neurones. Using this technique together with recordings of tail flick latency (TFL) elicited from lightly anaesthetised rats we have found that the specific 5-HT1a agonist 8-OH DPAT (15, 150, 300 nmol) increases nociceptive responses recorded from single dorsal horn neurones and decreases TFL. The non-specific 5-HT1b agonist TFMPP (300 nmol) and the general 5-HT1 agonist 5-CT (0.3, 3.0, 30 nmol) both decreased nociceptive responses and has inconsistent effects on TFL. Intrathecally applied 5-HT (130, 260 nmol) generally reduced nociceptive neuronal responses and increased TFL. In a minority of experiments, however, 5-HT increased nociceptive responses and it is suggested that this effect is associated with activation of 5-HT1a receptors. Activity at 5-HT1b receptors has the effect of suppressing or reducing responsiveness. The increased responsiveness of dorsal horn neurones to noxious stimulation associated with activity at 5-HT1a receptors may be associated either with increases in receptive field size, promotion of spinal nocifensive reflexes or the facilitation of the rostral transmission to specific brainstem sites.