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核心技术专利：CN118964589B侵权必究

核心技术专利：CN118964589B侵权必究

Calcagnetti D J, Schechter M D

Department of Pharmacology, Northeastern Ohio Universities College of Medicine, Rootstown.

Prog Neuropsychopharmacol Biol Psychiatry. 1993 Jul;17(4):637-49. doi: 10.1016/0278-5846(93)90011-g.

The objective of Exp. 1 was to determine whether intracerebroventricular (ICV) injection of cathinone CATH (8.0-32 micrograms) would produce a dose-dependent conditioned place preference (CPP) and/or activation in rats. Results indicate that rats conditioned with 16 or 32 micrograms doses of CATH significantly increased the time spent in their less preferred side, whereas rats conditioned with the 8.0 micrograms dose failed to show any shift from baseline preference. The 16 and 32 micrograms doses of CATH also significantly (p < .004) increased activity by more than 65% of baseline. 2. Exp. 2 was designed to determine whether ICV pretreatment with a dopamine release inhibitor CGS 10746B (CGS; 15 micrograms/rat) would block place conditioning produced by CATH. The results demonstrate that CGS pretreatment effectively blocked CATH-induced place conditioning and the CATH-induced elevation of activity.

实验1的目的是确定脑室内（ICV）注射卡西酮（CATH，8.0 - 32微克）是否会在大鼠中产生剂量依赖性条件性位置偏爱（CPP）和/或激活作用。结果表明，用16或32微克剂量的CATH进行条件化的大鼠，在其较不偏爱的一侧停留的时间显著增加，而用8.0微克剂量进行条件化的大鼠未表现出与基线偏爱有任何偏差。16和32微克剂量的CATH还使活动量显著（p <.004）增加，超过基线的65%。2. 实验2旨在确定用多巴胺释放抑制剂CGS 10746B（CGS，15微克/大鼠）进行ICV预处理是否会阻断CATH产生的位置条件化。结果表明，CGS预处理有效地阻断了CATH诱导的位置条件化以及CATH诱导的活动量升高。

Calcagnetti D J, Schechter M D

Department of Pharmacology, Northeastern Ohio Universities College of Medicine, Rootstown.

Prog Neuropsychopharmacol Biol Psychiatry. 1993 Jul;17(4):637-49. doi: 10.1016/0278-5846(93)90011-g.

The objective of Exp. 1 was to determine whether intracerebroventricular (ICV) injection of cathinone CATH (8.0-32 micrograms) would produce a dose-dependent conditioned place preference (CPP) and/or activation in rats. Results indicate that rats conditioned with 16 or 32 micrograms doses of CATH significantly increased the time spent in their less preferred side, whereas rats conditioned with the 8.0 micrograms dose failed to show any shift from baseline preference. The 16 and 32 micrograms doses of CATH also significantly (p < .004) increased activity by more than 65% of baseline. 2. Exp. 2 was designed to determine whether ICV pretreatment with a dopamine release inhibitor CGS 10746B (CGS; 15 micrograms/rat) would block place conditioning produced by CATH. The results demonstrate that CGS pretreatment effectively blocked CATH-induced place conditioning and the CATH-induced elevation of activity.

实验1的目的是确定脑室内（ICV）注射卡西酮（CATH，8.0 - 32微克）是否会在大鼠中产生剂量依赖性条件性位置偏爱（CPP）和/或激活作用。结果表明，用16或32微克剂量的CATH进行条件化的大鼠，在其较不偏爱的一侧停留的时间显著增加，而用8.0微克剂量进行条件化的大鼠未表现出与基线偏爱有任何偏差。16和32微克剂量的CATH还使活动量显著（p <.004）增加，超过基线的65%。2. 实验2旨在确定用多巴胺释放抑制剂CGS 10746B（CGS，15微克/大鼠）进行ICV预处理是否会阻断CATH产生的位置条件化。结果表明，CGS预处理有效地阻断了CATH诱导的位置条件化以及CATH诱导的活动量升高。