Transient Receptor Potential Vanilloid Type 1 Channel May Modulate Opioid Reward

Nguyen, Thi-Lien; Kwon, Seung-Hwan; Hong, Sa-Ik; Ma, Shi-Xun; Jung, Younghun; Hwang, Ji-Young; Kim, Hyoung‐Chun; Lee, Seok‐Yong; Jang, Choon‐Gon

doi:10.1038/npp.2014.90

Cited by 38 publications

(33 citation statements)

References 40 publications

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“…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). In a rat model of cocaine addiction, a TRPV1 receptor antagonist decreases cocaine-seeking behavior in the reinstatement phase, although TRPV1 seems to be unnecessary for the rewarding effect of cocaine (3).…”

Section: Rewardmentioning

confidence: 96%

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

Ligresti¹,

Petrocellis²,

Marzo³

2016

Physiological Reviews

378

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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Section: Rewardmentioning

confidence: 96%

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

Ligresti¹,

Petrocellis²,

Marzo³

2016

Physiological Reviews

378

337

View full text Add to dashboard Cite

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“…In addition to these activators, TRPV1 levels in DRG neurons were increased by nerve growth factor and the activation of p38 mitogen-activated protein kinase in inflamed skin [ 38 ]. It has also been suggested that the TRPV1 channel is activated by phosphatidylinositol 3-kinase-induced heat hyperalgesia [ 39 , 40 ]. In addition, the TRPV1 channel is activated by low pH [ 41 , 42 ].…”

Section: Trp Channelsmentioning

confidence: 99%

TRPV1 Channel: A Potential Drug Target for Treating Epilepsy

Nazıroğlu

2015

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Epilepsy has 2-3% incidence worldwide. However, present antiepileptic drugs provide only partial control of seizures. Calcium ion accumulation in hippocampal neurons has long been known as a major contributor to the etiology of epilepsy. TRPV1 is a calcium-permeable channel and mediator of epilepsy in the hippocampus. TRPV1 is expressed in epileptic brain areas such as CA1 area and dentate gyrus of the hippocampus. Here the author reviews the patent literature on novel molecules targeting TRPV1 that are currently being investigated in the laboratory and are candidates for future clinical evaluation in the management of epilepsy. A limited number of recent reports have implicated TRPV1 in the induction or treatment of epilepsy suggesting that this may be new area for potential drugs targeting this debilitating disease. Thus activation of TRPV1 by oxidative stress, resiniferatoxin, cannabinoid receptor (CB1) activators (i.e. anandamide) or capsaicin induced epileptic effects, and these effects could be reduced by appropriate inhibitors, including capsazepine (CPZ), 5'-iodoresiniferatoxin (IRTX), resolvins, and CB1 antagonists. It has been also reported that CPZ and IRTX reduced spontaneous excitatory synaptic transmission through modulation of glutaminergic systems and desensitization of TRPV1 channels in the hippocampus of rats. Immunocytochemical studies indicated that TRPV1 channel expression increased in the hippocampus of mice and patients with temporal lobe epilepsyTaken together, findings in the current literature support a role for calcium ion accumulation through TRPV1 channels in the etiology of epileptic seizures, indicating that inhibition of TRPV1 in the hippocampus may possibly be a novel target for prevention of epileptic seizures.

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“…Previous evidence showed that positive modulation of the TRPV1 channels could be a potential target for mitigation of AD (Jayant et al, 2016), suggesting an important involvement of TRPV1 in AD. In addition, Nguyen et al (2014) have also shown that TRPV1 plays a key role in morphine addiction. Blednov and Harris (2009) showed that the deletion of TRPV1 in mice altered behavioral effects of ethanol which indicates a connection between TRPV1 and alcoholism.…”

Section: Application Of Cmm To Two Gwas Data Sets For Ad and Sudsmentioning

confidence: 98%

Coupled Mixed Model for Joint Genetic Analysis of Complex Disorders with Two Independently Collected Data Sets

Wang

Pei

Vanyukov

et al. 2018

Preprint

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In the last decade, Genome-wide Association studies (GWASs) have contributed to decoding the human genome by uncovering many genetic variations associated with various diseases. Many followup investigations involve joint analysis of multiple independently generated GWAS data sets. While most of the computational approaches developed for joint analysis are based on summary statistics, the joint analysis based on individual-level data with consideration of confounding factors remains to be a challenge. In this study, we propose a method, called Coupled Mixed Model (CMM), that enables a joint GWAS analysis on two independently collected sets of GWAS data with different phenotypes. The CMM method does not require the data sets to have the same phenotypes as it aims to infer the unknown phenotypes using a set of multivariate sparse mixed models. Moreover, CMM addresses the confounding variables due to population stratication, family structures, and cryptic relatedness, as well as those arising during data collection such as batch effects that frequently appear in joint genetic studies. We evaluate the performance of CMM using simulation experiments. In real data analysis, we illustrate the utility of CMM by an application to evaluating common genetic associations for Alzheimers disease and substance use disorder using datasets independently collected for the two complex human disorders. Comparison of the results with those from previous experiments and analyses supports the utility of our method and provides new insights into the diseases. The software is available at https://github.com/HaohanWang/CMM

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Transient Receptor Potential Vanilloid Type 1 Channel May Modulate Opioid Reward

Cited by 38 publications

References 40 publications

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

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

TRPV1 Channel: A Potential Drug Target for Treating Epilepsy

Coupled Mixed Model for Joint Genetic Analysis of Complex Disorders with Two Independently Collected Data Sets

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