Involvement of CB1 receptors in the ventral tegmental area in the potentiation of morphine rewarding properties in acquisition but not expression in the conditioned place preference model

Rashidy-Pour, Ali; Pahlevani, Pouyan; Vaziri, Anoumid; Shaigani, Pariya; Zarepour, Leila; Vafaei, Abbas Ali; Haghparast, Abbas

doi:10.1016/j.bbr.2013.03.015

Cited by 26 publications

(16 citation statements)

References 48 publications

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“…It is clear that both exercise and drug addiction change the intracellular level of neurotransmitters. For example, extracellular levels of norepinephrine and glutamate decrease in the bed nucleus in chronic morphine-treated rats (17, 18). Morphine, like other drugs that have abuse liability, increases extracellular dopamine levels in the nucleus accumbens when administered systematically, or infused directly into mPFC (19-21).…”

Section: Discussionmentioning

confidence: 99%

Effect of Treadmill Running on Morphine Dependence Before and After Medial Prefrontal Cortex Lesion in Rats

Marghmaleki

Alaei

2016

Asian J Sports Med

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BackgroundPrevious studies on the medial prefrontal cortex (mPFC) has shown that this area plays an important role in addiction behavior. Other studies also indicated that exercise decreases use of morphine.ObjectivesThe aim of this study was to evaluate the effects of short-term exercise on trends for use of morphine with an intact mPFC and lesion of that area.Methods50 rats randomly were selected and divided into 5 groups. 1-exercise. 2- Morphine + Lesion. 3- Morphine + Exercise + Lesion. 4- Morphine. 5- Morphine and Exercise. All groups received morphine for 9 days except exercise group. On the 10th day, the symptoms of addiction were evaluated. To determine the effects of exercise, a treadmill apparatus was used for exercising.ResultsOur results indicated that exercise with intact mPFC area significantly decreased the tendency of using morphine which is verified by changes in symptoms (P < 0.05), but after a lesion of this area exercise did not significantly affect these withdrawal symptomsConclusionsIt seems that a lesion of mPFC area significantly reduced the effect of short-term exercise on the usage pattern of morphine.

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Section: Discussionmentioning

confidence: 99%

Effect of Treadmill Running on Morphine Dependence Before and After Medial Prefrontal Cortex Lesion in Rats

Marghmaleki

Alaei

2016

Asian J Sports Med

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“…Bellocchio et al, 2013; Rashidy-Pour et al, 2013), but results showing that this solvent can alter the analgesic activity of intracerebral morphine (Fossum et al, 2008) suggest caution in this use of DMSO. Presently, DMSO was used to dissolve CC44 in some experiments, but it is unlikely that use of this solvent invalidated the present conclusions.…”

Section: Discussionmentioning

confidence: 99%

Antinociceptive activity of CC44, a biotinylated improgan congener

Hoerbelt

Nalwalk

Phillips³

et al. 2013

European Journal of Pharmacology

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Improgan, a non-opioid, antinociceptive drug, activates descending analgesic circuits following brain administration, but the improgan receptor remains unidentified. Since biotinylation of drugs can enhance drug potency or facilitate discovery of new drug targets, a biotinylated congener of improgan (CC44) and several related compounds were synthesized and tested for antinociceptive activity. In rats and mice, intracerebroventricular (i.c.v.) administration of CC44 produced dose-dependent reductions in thermal nociceptive (tail flick and hot plate) responses, with 5-fold greater potency than improgan. CC44 also robustly attenuated mechanical (tail pinch) nociception in normal rats and mechanical allodynia in a spinal nerve ligation model of neuropathic pain. Similar to the effects of improgan, CC44 antinociception was reversed by the GABAA agonist muscimol (consistent with activation of analgesic circuits), and was resistant to the opioid antagonist naltrexone (implying a non-opioid mechanism). Also like improgan, CC44 produced thermal antinociception when microinjected into the rostral ventromedial medulla (RVM). Unlike improgan, CC44 (i.c.v.) produced antinociception which was resistant to antagonism by the cannabinoid CB1 antagonist/inverse agonist rimonabant. CC44 was inactive in mice following systemic administration, indicating that CC44 does not penetrate the brain. Preliminary findings with other CC44 congeners suggest that the heteroaromatic nucleus (imidazole), but not the biotin moiety, is required for CC44’s antinociceptive activity. These findings demonstrate that CC44 is a potent analgesic compound with many improgan-like characteristics. Since powerful techniques are available to characterize and identify the binding partners for biotin-containing ligands, CC44 may be useful in searching for new receptors for analgesic drugs.

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“…Dopaminergic transmission in VTA-NAc circuits can be modulated by effects of morphine treatment via cannabinoid and cholinergic systems ( Cossu et al, 2001 ; Karimi et al, 2013 ; Khaleghzadeh-Ahangar and Haghparast, 2015 ; Melis et al, 2000 ; Rashidy-Pour et al, 2013 ; Rezayof et al, 2008 ). For example, Tanda et al (1997) suggested that cannabinoids can activate VTA-NAc dopaminergic transmission by a common MOR-dependent mechanism shared with opioids, suggesting the possibility of crosstalk between cannabinoid and morphine signaling pathways.…”

Section: Ventral Tegmental Area (Vta)-nucleus Accumbens (Nac) Circuitmentioning

confidence: 99%

Brain Reward Circuits in Morphine Addiction

Kim

Ham

Hong

et al. 2016

Molecules and Cells

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Morphine is the most potent analgesic for chronic pain, but its clinical use has been limited by the opiate’s innate tendency to produce tolerance, severe withdrawal symptoms and rewarding properties with a high risk of relapse. To understand the addictive properties of morphine, past studies have focused on relevant molecular and cellular changes in the brain, highlighting the functional roles of reward-related brain regions. Given the accumulated findings, a recent, emerging trend in morphine research is that of examining the dynamics of neuronal interactions in brain reward circuits under the influence of morphine action. In this review, we highlight recent findings on the roles of several reward circuits involved in morphine addiction based on pharmacological, molecular and physiological evidences.

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Involvement of CB1 receptors in the ventral tegmental area in the potentiation of morphine rewarding properties in acquisition but not expression in the conditioned place preference model

Cited by 26 publications

References 48 publications

Effect of Treadmill Running on Morphine Dependence Before and After Medial Prefrontal Cortex Lesion in Rats

Effect of Treadmill Running on Morphine Dependence Before and After Medial Prefrontal Cortex Lesion in Rats

Antinociceptive activity of CC44, a biotinylated improgan congener

Brain Reward Circuits in Morphine Addiction

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