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Central glucocorticoid receptors modulate the expression of spinal cannabinoid receptors induced by chronic morphine exposure.
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Central cannabinoid receptors (CBRs) have been implicated in the opioid analgesic effects. However, it remains unclear as to whether the expression of central CBRs would be altered after repeated morphine exposure. Here, we show that chronic intrathecal treatment with morphine (10 microg, twice
Lack of morphine-induced dopamine release in the nucleus accumbens of cannabinoid CB(1) receptor knockout mice.
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Morphine (10 and 20 mg/kg, s.c.) does not modify dopamine release in the nucleus accumbens of cannabinoid CB(1) knock-out mice under conditions where it dose-dependently stimulates the release of dopamine in the corresponding wild-type mice. These results demonstrate that cannabinoid CB(1)
Contribution of spinal 5-HT5A receptors to the antinociceptive effects of systemically administered cannabinoid agonist WIN 55,212-2 and morphine.
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The antinociceptive effects of cannabinoids and opioids have been known for centuries. Serotonin and its receptors are also known to play important roles in nociception. However, the contribution of spinal 5-HT5A receptors in antinociceptive effects of cannabinoids and opioids has not been studied.
Interactive effects of morphine and nicotine on memory function depend on the central amygdala cannabinoid CB1 receptor function in rats.
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The present study investigated the possible involvement of the central amygdala (CeA) cannabinoid receptors type-1 (CB1Rs) in the interactive effects of morphine and nicotine on memory formation in a passive avoidance learning task. Our results showed that systemic administration of morphine (3 and
Topical cannabinoid enhances topical morphine antinociception.
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Opioids and cannabinoids produce antinociception through both spinal and supraspinal action. Both opioids and cannabinoids also have important peripheral action. Many previous studies indicate that systemically administered cannabinoids enhance antinociceptive properties of opioids. Experiments were
Pre-exposure to the cannabinoid receptor agonist CP 55940 enhances morphine behavioral sensitization and alters morphine self-administration in Lewis rats.
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Three experiments examined the influence of pre-exposure to the cannabinoid receptor agonist CP 55940 ((-)-cis-3-(2-hydroxy-4-(1,1-dimethylheptyl)phenyl)-trans-4-(3-hydroxypropyl)cyclohexanol) on the sensitization of morphine-induced locomotor hyperactivity and self-administration in Lewis rats. In
Cannabinoid receptor modulation changes the accumbal neuronal responses to morphine in the reinstatement of morphine-induced conditioned place preference.
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The nucleus accumbens (NAc) is a central component of the brain reward system. It has been known that most of the drugs of abuse such as opioids and cannabinoids affect the NAc. Although cannabinoids can modulate different stages of morphine encounter such as the reinstatement of morphine-induced
Cannabinoid agonist-induced sensitisation to morphine place preference in mice.
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The influence of the endocannabinoid system on the sensitisation to the rewarding effects of morphine in the place conditioning paradigm was evaluated. In mice pretreated with morphine this drug induces place preference with lower doses. Pretreatment with non-rewarding doses of the cannabinoid
Conditioned place preference to morphine in cannabinoid CB1 receptor knockout mice.
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Recent reports have suggested an involvement of the brain cannabinoid system in the morphine-reward pathway. To address this question we evaluated whether CB1 receptor knockout mice would show a conditioned place preference to morphine. CB1 receptor knockout mice developed a strong place preference
Modulation of rat brain cannabinoid receptors after chronic morphine treatment.
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Intraperitoneal injection of delta9-THC (7.5 mg/kg) in rats made tolerant to morphine by s.c. implantation of morphine pellets had a much greater analgesic effect than in placebo pellet plus delta9-THC treatment. To investigate whether this was due to some change in cannabinoid receptor levels
Effect of some cannabinoids on naloxone-precipitated abstinence in morphine-dependent mice.
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Mice were rendered morphine-dependent by the subcutaneous implantation of a pellet containing 75 mg of morphine base; 72 h after the implantation, the animals were injected intraperitoneally either with vehicle or with various doses of delta9-tetrahydrocannabinol, delta8-tetrahydrocannabinol,
GABA-cannabinoid interplays in the dorsal hippocampus and basolateral amygdala mediate morphine-induced amnesia.
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The aim of the current study was to investigate the involvement of GABA neurotransmission in the CA1 region and endocannabinoid system in the basolateral amygdala (BLA) on morphine-induced memory impairment. We hypothesized that possible functional interaction between the GABAergic and cannabinoid
Effects of Cannabinoid Type 2 Receptor Agonist AM1241 on Morphine-Induced Antinociception, Acute and Chronic Tolerance, and Dependence in Mice.
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Morphine is a potent opioid analgesic used to alleviate moderate or severe pain, but the development of drug tolerance and dependence limits its use in pain management. Previous studies showed that cannabinoid type 2 (CB2) receptor ligands may modulate opioid effects. However, there is no report of
Modulation of morphine and alcohol motor stimulant effects by cannabinoid receptors ligands.
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Previous studies evidenced in rats the suppression by cannabinoids of motor stimulant effects of various drugs of abuse. Here we investigated, in mice, the effects of an acute or a chronic administration with the cannabinoid agonist HU 210 on the motor stimulant effects of either morphine or
Basolateral amygdala CB1 cannabinoid receptors are involved in cross state-dependent memory retrieval between morphine and ethanol.
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Ethanol and morphine are largely co-abused and affect memory formation. The present study intended to investigate the involvement of cannabinoid CB1 receptors of the basolateral amygdala (BLA) in cross state-dependent memory retrieval between morphine and ethanol. Adult male Wistar rats received
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