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首页> 外文期刊>Pharmacology, Biochemistry and Behavior >Behavioral effects of dopamine agonists and antagonists in MPTP-lesioned D3 receptor knockout mice.
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Behavioral effects of dopamine agonists and antagonists in MPTP-lesioned D3 receptor knockout mice.

机译：多巴胺激动剂和拮抗剂对MPTP损伤的D3受体敲除小鼠的行为影响。

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To test the modulatory role of D(3) receptors in normal and dopamine-depleted mice, D(3) receptor KO mice and wild-type (WT) littermates were administered saline, L-dopa/carbidopa (20/2 mg/kg ip), a preferential D(3)>D(2) agonist S32504, a D1+D(2)/D(3) agonist apomorphine, a selective D(3) antagonist S33084, or apomorphine with S33084 prior to and after administration of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). We monitored lines crossed in a 55-min session, average number of rears, and average number of grooming bouts. MPTP treatment produced equivalent 70% losses of dopamine fibers in the caudate putamen (CPu) and nucleus accumbens (NAC) of WT and D(3) KO mice as compared to their control (vehicle injected) counterparts. D(3) receptors were absent in KO mice, and the number of D(3) receptors was unaffected by MPTP-induced loss of DA terminals in WT mice. The results support a lack of involvement of the D(3) receptor for D1:D2 receptor-mediated behavioral activity (synergy). First, S32504 inhibited all behaviors and to a similar degree in D(3) KO and WT mice. Second, S33084 at the higher concentration increased number of lines crossed in response to high dose apomorphine in both D(3) KO and WT mice. Third, in nonlesioned mice, apomorphine-induced gnawing stereotypies were inhibited by S33084 in both D(3) KO and WT mice. Interestingly, the inhibition of apomorphine-induced gnawing was not apparent in MPTP-lesioned mice, and this stereotypy was elevated in D(3) KO-MPTP-lesioned mice. Thus, the suppressive effects of S32504 could be via D2 autoreceptor inhibition of DA release, and D2 receptor blockade by S33084 leads to release of that inhibition. This may be more apparent in MPTP-lesioned partially DA denervated mice.
机译：为了测试D（3）受体在正常和多巴胺耗尽的小鼠中的调节作用，向D（3）受体KO小鼠和野生型（WT）同窝仔小鼠施用生理盐水，L-多巴/卡比多巴（20/2 mg / kg ip），优先D（3）> D（2）激动剂S32504，D1 + D（2）/ D（3）激动剂阿扑吗啡，选择性D（3）拮抗剂S33084或阿扑吗啡与S33084给药前后1-甲基-4-苯基-1，2，3，6-四氢吡啶（MPTP）。我们监控了55分钟内的划线，平均后排次数和平均修饰次数。 MPTP处理与野生型和D（3）KO小鼠的尾状壳核（CPu）和伏隔核（NAC）相比，它们的对照（注射车辆）对应的多巴胺纤维损失了70％。 D（3）受体在KO小鼠中不存在，并且D（3）受体的数量不受WT小鼠中MPTP诱导的DA末端丢失的影响。结果支持缺乏参与D1：D2受体介导的行为活性（协同作用）的D（3）受体。首先，S32504抑制了所有行为，并在D（3）KO和WT小鼠中达到了相似的程度。其次，在D（3）KO和WT小鼠中，较高浓度的S33084会增加响应高剂量阿扑吗啡的交叉线数。第三，在非病变小鼠中，D330（3）KO和WT小鼠均受S33084抑制阿扑吗啡诱导的刻板印象。有趣的是，阿扑吗啡诱导的咬伤的抑制作用在MPTP损伤的小鼠中并不明显，而这种定型性在D（3）KO-MPTP损伤的小鼠中升高。因此，S32504的抑制作用可能是通过D2自受体抑制DA释放，而S33084对D2受体的阻断导致了该抑制的释放。这在MPTP损伤的部分DA去神经支配的小鼠中可能更明显。

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