DIFFERENT ROLE OF 5-HT1A AND 5-HT2 RECEPTORS IN SPINAL-CORD IN THE CONTROL OF NOCICEPTIVE RESPONSIVENESS

DIFFERENT ROLE OF 5-HT1A AND 5-HT2 RECEPTORS IN SPINAL-CORD IN THE CONTROL OF NOCICEPTIVE RESPONSIVENESS
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DOI:
10.1016/0028-3908(91)90180-j
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发表时间:
1991-07-01
期刊:
影响因子:
4.7
通讯作者:
HOLE, K
HOLE, K
中科院分区:
医学2区
文献类型:
--
作者:
EIDE, PK;HOLE, K

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比较了5-羟色胺2型(5-HT 2)受体激动剂(+/-)-1-(2,5-二甲氧基-4-碘苯基)-2-氨基丙烷(DOI)和5-HT 1A激动剂(+)-8-羟基-2-(二正丙基氨基)-四氢萘[(+)-8-OH-DPAT]对小鼠伤害性反应的影响。鞘内注射DOI(5-20 μ g)可产生剂量依赖性行为综合征,包括咬或舔身体尾部和相互的后肢抓挠。然而,(+)-8-OH-DPAT(5-20 μ g)不产生咬和抓行为。用P物质受体拮抗剂[D-Arg 1,D-Trp 7,9,Leu 11]-SP(Spantide)(5 μ g)处理可逆转对DOI(20 μ g)的反应。注射(+)-8-OH-DPAT后5-20 min,甩尾反射明显减弱; DOI注射后5 min,甩尾反射无明显改变,但注射后10-20 min,甩尾反射明显减弱。数据表明,5-HT 2受体的刺激,而不是5-HT 1A受体,诱导的行为综合征,这可能反映了伤害性通路的激活。刺激5-HT_(1A)受体比刺激5-HT_(2)受体对甩尾反射的抑制作用更明显。因此,5-HT 2和5-HT 1A受体似乎在调节小鼠的伤害感受性反应中具有不同的功能。
The effects of the 5-hydroxytryptamine type-2 (5-HT2) receptor agonist (+/-)-1-(2,5-dimethoxy-4-iodophenyl)-2-aminopropane (DOI) and the 5-HT1A agonist (+)-8-hydroxy-2-(di-n-propylamino)-tetralin [(+)-8-OH-DPAT] on nociceptive responsiveness were compared in mice. Intrathecal administration of DOI (5-20-mu-g) produced a dose-dependent behavioural syndrome, consisting of biting or licking, directed towards the caudal part of the body and reciprocal hindlimb scratching. However, (+)-8-OH-DPAT (5-20-mu-g) did not produce the biting and scratching behaviour. The response to DOI (20-mu-g) was reversed by treatment with the substance P receptor antagonist, [D-Arg 1, D-Trp 7,9, Leu 11]-SP (Spantide) (5-mu-g). The tail-flick reflex was markedly depressed 5-20 min after administration of (+)-8-OH-DPAT; DOI did not change the tail-flick reflex after 5 min but significantly inhibited the reflex response 10-20 min after injection. The data show that stimulation of 5-HT2 receptors, but not 5-HT1A receptors, induced a behavioural syndrome, which may reflect activation of nociceptive pathways. The tail-flick reflex was more markedly inhibited by stimulation of 5-HT1A than 5-HT2 receptors. Accordingly, 5-HT2 and 5-HT1A receptors seem to have a different function in the modulation of nociceptive responsiveness in the mouse.