Ferrari F, Ottani A, Giuliani D
Department of Biomedical Sciences, University of Modena and Reggio Emilia, Modena, Italy.
Life Sci. 1999;65(8):823-31. doi: 10.1016/s0024-3205(99)00309-4.
Acute injection of the cannabinoid agonist HU 210 (6.25-100 microg/kg, i.p.) dose-dependently inhibited rat locomotor activity and rearing, while subchronic treatment with the drug (once daily for 7 days) at the same doses only diminished locomotion. Acute but not subchronic administration of HU 210 (12.5-50 microg/kg, i.p.) potently counteracted acute and subchronic cocaine (15 mg/kg, i.p.)-induced hyperlocomotion and enhanced rearing. The acute cannabinoid (6.25-100 microg/kg, i.p.) also inhibited locomotor activity, stereotyped behaviour and shaking elicited by the D1/D2 agonist CQP 201-403 (500 microg/kg, i.p.). On the contrary, subchronic treatments with HU 210 enhanced CQP 201-403-induced locomotor activity and potently stimulated escape attempts. Discussion centers on the influence of cannabinoids on experimental models of psychosis.
急性注射大麻素激动剂HU 210（6.25 - 100微克/千克，腹腔注射）可剂量依赖性地抑制大鼠的运动活性和竖毛行为，而以相同剂量对大鼠进行亚慢性给药（每日一次，共7天）仅会减少其运动量。急性而非亚慢性给予HU 210（12.5 - 50微克/千克，腹腔注射）可有效对抗急性和亚慢性可卡因（15毫克/千克，腹腔注射）诱导的运动亢进并增强竖毛行为。急性大麻素（6.25 - 100微克/千克，腹腔注射）还可抑制由D1/D2激动剂CQP 201 - 403（500微克/千克，腹腔注射）引发的运动活性、刻板行为和震颤。相反，HU 210的亚慢性给药增强了CQP 201 - 403诱导的运动活性，并有力地刺激了逃避尝试。讨论集中在大麻素对精神病实验模型的影响上。
