Verma A, Kulkarni S K, Nayar U
Department of Pharmaceutical Sciences, Panjab University, Chandigarh, India.
Methods Find Exp Clin Pharmacol. 1993 Oct;15(8):515-25.
The effect of selective D1- and D2-dopamine (DA) receptor stimulation on neocortical and hippocampal electroencephalographic (EEG) activity of rat brain was studied. The modulation of the effect of rimcazole, a sigma receptor antagonist, by D1- and D2-DA receptor agonists was also investigated. B-HT 920 (0.5 mg/kg), a D2 DA agonist, produced significant inhibition of EEG activity in neocortex and hippocampus. The lower doses of B-HT 920 (0.1 and 0.25 mg/kg) either enhanced the frequency and amplitude of cortical and hippocampal firing or lacked any significant effect. The inhibitory effect of B-HT 920 was blocked by haloperidol (0.5 mg/kg), a D2-receptor antagonist and enhanced by idazoxan (1.0 mg/kg), an alpha 2-adrenoceptor antagonist. SKF 38393 (5.0 mg/kg), a D1-DA receptor agonist and dopamine (10 mcg/rat) or apomorphine (0.5 mg/kg), a mixed D1-/D2-agonist, also inhibited the frequency and amplitude of cortical and hippocampal EEG. A significantly higher inhibition of electrical activity was observed following concomitant administration of B-HT 920 (0.1 mg/kg) and SKF 38393 (5.0 mg/kg) in comparison with the effect of each drug alone. Rimcazole (6.0 mg/kg) increased the frequency of cortical and hippocampal firing. Amplitude of cortical firing was enhanced but not of hippocampal EEG following administration of rimcazole. Rimcazole blocked the effect of SKF 38393 (5.0 mg/kg) and apomorphine (0.5 mg/kg) but not of B-HT 920 (0.5 mg/kg) on cortical and hippocampal EEG, respectively. The above data suggests a modulatory effect of D1-receptor activation on the inhibitory effect of D2-receptor stimulation in cortex as well as hippocampus and the blockade by rimcazole of the effect of D1-DA receptor agonist in these areas.
研究了选择性刺激 D1 和 D2 多巴胺(DA)受体对大鼠大脑新皮质和海马脑电图(EEG)活动的影响。还研究了西格玛受体拮抗剂利米唑的作用受 D1 和 D2 DA 受体激动剂调节的情况。D2 DA 激动剂 B-HT 920(0.5 毫克/千克)对新皮质和海马的 EEG 活动产生了显著抑制。较低剂量的 B-HT 920(0.1 和 0.25 毫克/千克)要么提高了皮质和海马放电的频率和幅度,要么没有任何显著影响。B-HT 920 的抑制作用被 D2 受体拮抗剂氟哌啶醇(0.5 毫克/千克)阻断,并被α2 肾上腺素能受体拮抗剂咪唑克生(1.0 毫克/千克)增强。D1-DA 受体激动剂 SKF 38393(5.0 毫克/千克)以及多巴胺(10 微克/大鼠)或混合 D1-/D2-激动剂阿扑吗啡(0.5 毫克/千克)也抑制了皮质和海马 EEG 的频率和幅度。与单独使用每种药物的效果相比,同时给予 B-HT 920(0.1 毫克/千克)和 SKF 38393(5.0 毫克/千克)后,观察到电活动的抑制作用明显更高。利米唑(6.0 毫克/千克)增加了皮质和海马放电的频率。给予利米唑后,皮质放电的幅度增强,但海马 EEG 的幅度未增强。利米唑分别阻断了 SKF 38393(5.0 毫克/千克)和阿扑吗啡(0.5 毫克/千克)对皮质和海马 EEG 的作用,但未阻断 B-HT 920(0.5 毫克/千克)的作用。上述数据表明,D1 受体激活对 D2 受体刺激在皮质和海马中的抑制作用具有调节作用,以及利米唑对这些区域中 D1-DA 受体激动剂作用的阻断。