Romero Eva M, Fernández Beatriz, Sagredo Onintza, Gomez Nuria, Urigüen Leyre, Guaza Carmen, De Miguel Rosario, Ramos Jose Antonio, Viveros M Paz
Departamento de Biología Animal II, Facultad de Biología, Universidad Complutense, 28040 Madrid, Spain.
Brain Res Dev Brain Res. 2002 Jun 30;136(2):85-92. doi: 10.1016/s0165-3806(02)00306-1.
The peripubertal period appears to be critical in relation to the abuse of cannabinoids and opioids in humans. However there is little information about the acute effects of cannabinoids and their interactions with opioids in young experimental animals. We have studied the effects of the cannabinoid agonist CP 55,940 (0.1, 0.2, 0.4 and 0.6 mg/kg) on the nociceptive responses (tail immersion test) and holeboard activity of 40-day-old rats, and the involvement of the CB(1) receptor (antagonism by SR 141716A, 3 mg/kg). The implication of the opioid system was evaluated using the opioid antagonist naloxone (1 mg/kg) and a combined treatment with subeffective doses of CP 55,940 (0.1 mg/kg) and morphine (1 mg/kg). The effects of CP 55,940 on the serum corticosterone levels (radioimmunoassay) and on the dopamine and DOPAC contents of discrete brain regions (high-performance liquid chromatography) were also assessed. The antinociceptive effect of CP 55,940 was of a similar magnitude at all the doses used. The results show the involvement of the CB(1) receptor. The cannabinoid agonist significantly depressed the holeboard activity in a dose-dependent manner. The results indicate that the CB(1) receptor is involved in the effects on motor activity but not in the effects on the exploratory activity. The behavioural effects of CP 55,940 were modulated by morphine. The cannabinoid agonist (0.6 mg/kg) induced a CB(1)-mediated increase in the serum corticosterone levels, but no effect on the dopaminergic systems of either the striatum or the limbic forebrain was found.
青春期前后这段时期似乎是人类滥用大麻素和阿片类药物的关键时期。然而，关于大麻素在幼年实验动物中的急性效应及其与阿片类药物的相互作用，目前所知甚少。我们研究了大麻素激动剂CP 55,940（0.1、0.2、0.4和0.6毫克/千克）对40日龄大鼠伤害性反应（尾浸试验）和洞板活动的影响，以及CB(1)受体的参与情况（用SR 141716A拮抗，3毫克/千克）。使用阿片类拮抗剂纳洛酮（1毫克/千克）以及CP 55,940（0.1毫克/千克）和吗啡（1毫克/千克）的亚有效剂量联合治疗来评估阿片系统的作用。还评估了CP 55,940对血清皮质酮水平（放射免疫测定）以及离散脑区多巴胺和DOPAC含量（高效液相色谱法）的影响。CP 55,940在所有使用剂量下的镇痛效果相似。结果表明CB(1)受体参与其中。大麻素激动剂以剂量依赖性方式显著抑制洞板活动。结果表明，CB(1)受体参与了对运动活动的影响，但未参与对探索活动的影响。CP 55,940的行为效应受到吗啡的调节。大麻素激动剂（0.6毫克/千克）诱导CB(1)介导的血清皮质酮水平升高，但未发现对纹状体或边缘前脑的多巴胺能系统有影响。
