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编 号：F015198
分子式：C50H67N11O11S2
分子量：1062.26
分子式：C50H67N11O11S2
分子量：1062.26
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CAS No: 103429-31-8
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CTOP is a potent and highly selective μ-opioid receptor antagonist. CTOP antagonizes the acute morphine-induced analgesic effect and hypermotility. CTOP enhances extracellular dopamine levels in the nucleus accumbens. CTOP dose-dependently enhances locomotor activity.
体内研究：
CTOP (0-0.5 nmol, ICV, once) antagonizes the analgesic effect of morphine in a dose-dependent manner.CTOP (0-2 nmol, ICV, once) causes withdrawal hypothermia and a loss of body weight in morphine-dependent animals.CTOP (0-1.5 nmol per side, Intra-VTA injection) enhances extracellular dopamine levels in the nucleus accumbens and dose-dependently enhances locomotor activity.Animal Model:Male CFLP mice (25-30 g)
Dosage:0, 0.001, 0.05, 0.075, 0.1, and 0.5 nmol (made up in artificial cerebrospinalfluid (CSF) and kept in plastic tubes at -25℃ until use)
Administration:Intracerebroventricular (i.c.v.) administration, once
Result:Antagonized the analgesic effect of morphine in a dose-dependent manner, antagonizedthe morphine-induced hypermotility in a dose-dependent manner.
Animal Model:Male CFLP mice (25-30 g, Acute dependence to morphine was induced by a single dependence-inducing (100 mg/kg) dose of morphine-HC1)
Dosage:0, 0.001, 0.05, 0.2, and 2 nmol
Administration:Intracerebroventricular (i.c.v.) administration, once
Result:Decreased the body temperature in a dose-dependent manner, and caused withdrawal hypothermia and a loss of body weight in morphine-dependent animals.
Animal Model:Long-Evans hooded rats (12, male, 350-450 g)
Dosage:0, 0.015, 0.15, and 1.5 nmol per side
Administration:Intra-VTA (ventral tegmental area) injection
Result:Enhanced extracellular dopamine levels in the nucleus accumbens, dose-dependently increased activity, whereas had no effect on feeding and drinking behavior.
CTOP is a potent and highly selective μ-opioid receptor antagonist. CTOP antagonizes the acute morphine-induced analgesic effect and hypermotility. CTOP enhances extracellular dopamine levels in the nucleus accumbens. CTOP dose-dependently enhances locomotor activity.
体内研究：
CTOP (0-0.5 nmol, ICV, once) antagonizes the analgesic effect of morphine in a dose-dependent manner.CTOP (0-2 nmol, ICV, once) causes withdrawal hypothermia and a loss of body weight in morphine-dependent animals.CTOP (0-1.5 nmol per side, Intra-VTA injection) enhances extracellular dopamine levels in the nucleus accumbens and dose-dependently enhances locomotor activity.Animal Model:Male CFLP mice (25-30 g)
Dosage:0, 0.001, 0.05, 0.075, 0.1, and 0.5 nmol (made up in artificial cerebrospinalfluid (CSF) and kept in plastic tubes at -25℃ until use)
Administration:Intracerebroventricular (i.c.v.) administration, once
Result:Antagonized the analgesic effect of morphine in a dose-dependent manner, antagonizedthe morphine-induced hypermotility in a dose-dependent manner.
Animal Model:Male CFLP mice (25-30 g, Acute dependence to morphine was induced by a single dependence-inducing (100 mg/kg) dose of morphine-HC1)
Dosage:0, 0.001, 0.05, 0.2, and 2 nmol
Administration:Intracerebroventricular (i.c.v.) administration, once
Result:Decreased the body temperature in a dose-dependent manner, and caused withdrawal hypothermia and a loss of body weight in morphine-dependent animals.
Animal Model:Long-Evans hooded rats (12, male, 350-450 g)
Dosage:0, 0.015, 0.15, and 1.5 nmol per side
Administration:Intra-VTA (ventral tegmental area) injection
Result:Enhanced extracellular dopamine levels in the nucleus accumbens, dose-dependently increased activity, whereas had no effect on feeding and drinking behavior.
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