Blocking TRPV1 in Nucleus Accumbens Inhibits Persistent Morphine Conditioned Place Preference Expression in Rats

Heng, Li-Jun; Huang, Bo; Guo, Hongzhu; Ma, Li; Yuan, Wei-Xin; Song, Jian; Wang, Peng; Xu, Guohai; Gao, Guodong

doi:10.1371/journal.pone.0104546

Cited by 20 publications

(12 citation statements)

References 48 publications

(66 reference statements)

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“…Regarding the blocking effect of PEA on cocaine-induced CPP expression observed in the present study, it was previously reported that the administration of a selective antagonist of TRPV1 in the nucleus accumbens was able to abolish the expression of morphine-induced CPP (Heng et al, 2014). Therefore, it seems unlikely that the activation of TRPV1 by PEA could underlie the abolishment of the CPP expression by PEA.…”

Section: The Blocking Effect Of Pea Administration On Expression Of Csupporting

confidence: 46%

Palmitoylethanolamide attenuates cocaine-induced behavioral sensitization and conditioned place preference in mice

Zambrana-Infantes

Rosell‐Valle

Guevara‐Miranda

et al. 2018

Pharmacology Biochemistry and Behavior

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Cocaine addiction is a chronically relapsing disorder characterized by compulsive drug-seeking and drug-taking behaviors. Previous studies have demonstrated that cocaine, as well as other drugs of abuse, alters the levels of lipid-based signaling molecules, such as N-acylethanolamines (NAEs). Moreover, brain levels of NAEs have shown sensitivity to cocaine self-administration and extinction training in rodents. Given this background, the aim of this study was to investigate the effects of repeated or acute administration of palmitoylethanolamide (PEA), an endogenous NAE, on psychomotor sensitization and cocaine-induced contextual conditioning. To this end, the potential ability of repeated PEA administration (1 or 10 mg/kg, i.p.) to modulate the acquisition of cocaine-induced behavioral sensitization (BS) and conditioned place preference (CPP) was assessed in male C57BL/6J mice. In addition, the expression of cocaine-induced BS and CPP following acute PEA administration were also studied. Results showed that repeated administration of both doses of PEA were able to block the acquisition of cocaine-induced BS. Furthermore, acute administration of both doses of PEA was able to abolish the expression of BS, while the highest dose also abolished the expression of cocaine-induced CPP. Taken together, these results indicate that exogenous administration of PEA attenuated psychomotor sensitization, while the effect of PEA in cocaine-induced CPP depended on whether PEA was administered repeatedly or acutely. These findings could be relevant to understand the role that NAEs play in processes underlying the development and maintenance of cocaine addiction.

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Section: The Blocking Effect Of Pea Administration On Expression Of Csupporting

confidence: 46%

Palmitoylethanolamide attenuates cocaine-induced behavioral sensitization and conditioned place preference in mice

Zambrana-Infantes

Rosell‐Valle

Guevara‐Miranda

et al. 2018

Pharmacology Biochemistry and Behavior

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“…TRPV1 affects -opioid receptor binding, which is increased by morphine and diminished by microinjection of capsazepine. It seems that other than in dorsal striatum, TRPV1 participates in morphine reward also in the cortex, nucleus accumbens, and ventral tegmental area (338). Further experimental data suggest that TRPV1 contributes to morphine reward via adenylyl cyclase 1, p38 MAPK, and NF-B (624).…”

Section: Rewardmentioning

confidence: 96%

“…In the dorsal striatum, repeated morphine treatments are able to upregulate TRPV1 gene expression, and the administration of the TRPV1 agonist capsaicin potentiates morphine reward, whereas microinjection of selective TRPV1 antagonists inhibit morphine-conditioned place preference (338). TRPV1 affects -opioid receptor binding, which is increased by morphine and diminished by microinjection of capsazepine.…”

Section: Rewardmentioning

confidence: 99%

From Phytocannabinoids to Cannabinoid Receptors and Endocannabinoids: Pleiotropic Physiological and Pathological Roles Through Complex Pharmacology

Ligresti¹,

Petrocellis²,

Marzo³

2016

Physiological Reviews

380

337

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Apart from having been used and misused for at least four millennia for, among others, recreational and medicinal purposes, the cannabis plant and its most peculiar chemical components, the plant cannabinoids (phytocannabinoids), have the merit to have led humanity to discover one of the most intriguing and pleiotropic endogenous signaling systems, the endocannabinoid system (ECS). This review article aims to describe and critically discuss, in the most comprehensive possible manner, the multifaceted aspects of 1) the pharmacology and potential impact on mammalian physiology of all major phytocannabinoids, and not only of the most famous one ⌬ 9 -tetrahydrocannabinol, and 2) the adaptive prohomeostatic physiological, or maladaptive pathological, roles of the ECS in mammalian cells, tissues, and organs. In doing so, we have respected the chronological order of the milestones of the millennial route from medicinal/recreational cannabis to the ECS and beyond, as it is now clear that some of the early steps in this long path, which were originally neglected, are becoming important again. The emerging picture is rather complex, but still supports the belief that more important discoveries on human physiology, and new therapies, might come in the future from new knowledge in this field.

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“…Its action upon TRPV1 may not mediate any therapeutic effects in addiction, AS blocking this channel turns out to be beneficial to control addictive behavior [285,286]. Equally, the roles of VDAC1, VGCCs, and the other TRP channels that are targets for CBD have not yet had their role in addiction firmly established.…”

Section: Cbd Ion Channel Targets In Addictionmentioning

confidence: 99%

Molecular Targets of Cannabidiol in Neurological Disorders

Bih

Chen

Nunn³

et al. 2015

Neurotherapeutics

464

323

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Cannabis has a long history of anecdotal medicinal use and limited licensed medicinal use. Until recently, alleged clinical effects from anecdotal reports and the use of licensed cannabinoid medicines are most likely mediated by tetrahydrocannabinol by virtue of: 1) this cannabinoid being present in the most significant quantities in these preparations; and b) the proportion:potency relationship between tetrahydrocannabinol and other plant cannabinoids derived from cannabis. However, there has recently been considerable interest in the therapeutic potential for the plant cannabinoid, cannabidiol (CBD), in neurological disorders but the current evidence suggests that CBD does not directly interact with the endocannabinoid system except in vitro at supraphysiological concentrations. Thus, as further evidence for CBD's beneficial effects in neurological disease emerges, there remains an urgent need to establish the molecular targets through which it exerts its therapeutic effects. Here, we conducted a systematic search of the extant literature for original articles describing the molecular pharmacology of CBD. We critically appraised the results for the validity of the molecular targets proposed. Thereafter, we considered whether the molecular targets of CBD identified hold therapeutic potential in relevant neurological diseases. The molecular targets identified include numerous classical ion channels, receptors, transporters, and enzymes. Some CBD effects at these targets in in vitro assays only manifest at high concentrations, which may be difficult to achieve in vivo, particularly given CBD's relatively poor bioavailability. Moreover, several targets were asserted through experimental designs that demonstrate only correlation with a given target rather than a causal proof. When the molecular targets of CBD that were physiologically plausible were considered for their potential for exploitation in neurological therapeutics, the results were variable. In some cases, the targets identified had little or no established link to the diseases considered. In others, molecular targets of CBD were entirely consistent with those already actively exploited in relevant, clinically used, neurological treatments. Finally, CBD was found to act upon a number of targets that are linked to neurological therapeutics but that its actions were not consistent withmodulation of such targets that would derive a therapeutically beneficial outcome. Overall, we find that while >65 discrete molecular targets have been reported in the literature for CBD, a relatively limited number represent plausible targets for the drug's action in neurological disorders when judged by the criteria we set. We conclude that CBD is very unlikely to exert effects in neurological diseases through modulation of the endocannabinoid system. Moreover, a number of other molecular targets of CBD reported in the literature are unlikely to be of relevance owing to effects only being observed at supraphysiological concentrations. Of interest and after excludin...

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Blocking TRPV1 in Nucleus Accumbens Inhibits Persistent Morphine Conditioned Place Preference Expression in Rats

Cited by 20 publications

References 48 publications

Palmitoylethanolamide attenuates cocaine-induced behavioral sensitization and conditioned place preference in mice

Palmitoylethanolamide attenuates cocaine-induced behavioral sensitization and conditioned place preference in mice

From Phytocannabinoids to Cannabinoid Receptors and Endocannabinoids: Pleiotropic Physiological and Pathological Roles Through Complex Pharmacology

Molecular Targets of Cannabidiol in Neurological Disorders

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