Yawning and locomotor behavior induced by dopamine receptor agonists in mice and rats.
Yawning and locomotor behavior induced by dopamine receptor agonists in mice and rats.
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DOI：
10.1097/fbp.0b013e32833a5c68
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发表时间：
2010-05
影响因子：
1.6
通讯作者：
Katz JL
中科院分区：
文献类型：
--
作者：
Li SM;Collins GT;Paul NM;Grundt P;Newman AH;Xu M;Grandy DK;Woods JH;Katz JL
多巴胺(DA)能激动剂诱导的大鼠打哈欠似乎是由DA D3受体介导的，低剂量的DA激动剂可降低大鼠的运动活动，这种作用归因于突触前D2受体。研究了几种DA激动剂对大鼠和小鼠打哈欠和运动活动的影响。打哈欠在老鼠身上是可靠的，在这两个物种中都是由胆碱能激动剂毒扁豆碱引起的。然而，DA激动剂对瑞士韦氏小鼠、DA D2R和DA D3R基因敲除小鼠或野生型小鼠的打哈欠无效。这些药物在一到两个低剂量时显著减少大鼠的运动活动，而在高剂量时活动恢复到对照水平。在小鼠中，这些药物在1000-10000倍的剂量范围内减少了活动，在最高剂量时，活性处于对照水平(U-91356A)或高于对照水平[(±)-7-羟基-2-二丙氨基四氢溴化铵，喹比罗]。低剂量激动剂使除DA D2R基因敲除小鼠外的所有小鼠的运动能力降低，但不能被DA D2R或D3R拮抗剂(L-741626、BP 897或PG01037)所拮抗。在小鼠中，打哈欠并不能提供体内DA D3R激动剂活性的选择性指标。DA激动剂降低小鼠的运动活性似乎是由D2DA受体介导的。
Dopaminergic (DA) agonist-induced yawning in rats seems to be mediated by DA D3 receptors, and low doses of several DA agonists decrease locomotor activity, an effect attributed to presynaptic D2 receptors. Effects of several DA agonists on yawning and locomotor activity were examined in rats and mice. Yawning was reliably produced in rats, and by the cholinergic agonist, physostigmine, in both the species. However, DA agonists were ineffective in producing yawning in Swiss–Webster or DA D2R and DA D3R knockout or wild-type mice. The drugs significantly decreased locomotor activity in rats at one or two low doses, with activity returning to control levels at higher doses. In mice, the drugs decreased locomotion across a 1000–10 000-fold range of doses, with activity at control levels (U-91356A) or above control levels [(±)-7-hydroxy-2-dipropylaminotetralin HBr, quinpirole] at the highest doses. Low doses of agonists decreased locomotion in all mice except the DA D2R knockout mice, but were not antagonized by DA D2R or D3R antagonists (L-741 626, BP 897, or PG01037). Yawning does not provide a selective in-vivo indicator of DA D3R agonist activity in mice. Decreases in mouse locomotor activity by the DA agonists seem to be mediated by D2 DA receptors.