Addiction

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Addiction 2018-08-01T21:46:00+00:00

Endocannabinoid-Enhanced “Liking” in Nucleus Accumbens Shell Hedonic Hotspot Requires Endogenous Opioid Signals

Marci R. Mitchell, Kent C. Berridge, and Stephen V. Mahler  (July 2018)
Stimulating either endogenous cannabinoids or opioids within a restricted dorsomedial “hedonic hotspot” in nucleus accumbens (NAc) shell enhances hedonic impact, or “liking” reactions to sweet tastes. In this study, we probed within this hotspot the relationship between endocannabinoid and opioid signals in hedonic enhancement. These results elaborate our understanding of the mechanisms of hedonic processing of food rewards, and may also carry implications more generally for how opioid and cannabinoid drugs interact to generate natural pleasures, or drug-induced euphoria.

Cannabidiol reverses attentional bias to cigarette cues in a human experimental model of tobacco withdrawal.

Hindocha C, Freeman TP, Grabski M, Stroud JB, Crudgington H, Davies AC, Das RK, Lawn W, Morgan CJA, Curran HV (May 2018)

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A single 800mg oral dose of cannabidiol (CBD) reduced the salience and pleasantness of cigarette cues, compared with placebo, after overnight cigarette abstinence in dependent smokers. CBD did not influence tobacco craving or withdrawal or any subjectively rated side-effects.


Acute and chronic modulation of striatal endocannabinoid‐mediated plasticity by nicotine

Louise Adermark, Julia Morud, Amir Lotfi, Mia Ericson, Bo Söderpalm  (January 2018)
Drug addiction is a chronic relapsing disorder that involves progressive adaptations of cortico‐striatal networks (Yin, Ostlund, & Balleine 2008; Belin et al. 2009; Belin et al. 2013; Adermark et al. 2016), and the data presented here suggest that the eCB system might play a role in mediating these transformations. Even though no causal relationship with behavioral transformations was assessed in this study, it is possible that nicotine‐induced facilitation of eCB signaling could promote neuroadaptations and contribute to the initial conditioning and motivational effects elicited by nicotine.

Epigenetic mechanisms associated with addiction-related behavioural effects of nicotine and/or cocaine: implication of the endocannabinoid system

Hayase, Tamaki (October 2017)

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The addictive use of nicotine (NC) and cocaine (COC) continues to be a major public health problem, and their combined use has been reported, particularly during adolescence. In neural plasticity, commonly induced by NC and COC, as well as behavioural plasticity related to the use of these two drugs, the involvement of epigenetic mechanisms, in which the reversible regulation of gene expression occurs independently of the DNA sequence, has recently been reported. This article presents the addiction-related behavioural effects of NC and/or COC, based on the common behavioural/neural plasticity and combined use of NC/COC, and reviews the interacting role of the ECB system.


Fatty acid amide hydrolase (FAAH) inactivation confers enhanced sensitivity to nicotine‐induced dopamine release in the mouse nucleus accumbens

Francisco J. Pavon, Antonia Serrano, Nimish Sidhpura, Ilham Polis, David Stouffer, Fernando Rodriguez de Fonseca, Benjamin F. Cravatt, Rémi Martin‐Fardon, Loren H. Parsons  (June 2017)
Nicotine exerts its rewarding effects by promoting an increase in dopamine (DA) release in the nucleus accumbens (NAc), and this process is influenced by the endocannabinoid system. Fatty acid amide hydrolase (FAAH) is the main enzyme responsible for the degradation of the endocannabinoid anandamide and other non‐cannabinoid N‐acylethanolamines. Previous research has reported that both genetic deletion and pharmacological inhibition of FAAH enhance nicotine‐induced conditioned place preference at low doses.

The endocannabinoid system as a target for addiction treatment: Trials and tribulations

Matthew E.SloanJoshua L.GowinVijay A.RamchandaniYasmin L.HurdBernardLe Foll (May 2017)

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Endocannabinoid signaling is involved in reward and addiction, which raises the possibility that drugs targeting this system could be used to treat substance use disorders. This review discusses findings from randomized controlled trials evaluating cannabinergic medications for addiction.


Endocannabinoid Signaling in Reward and Addiction: From Homeostasis to Pathology

Sarah A. Laredo, William R. Marrs, Loren H. Parsons  (May 2017)

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The endogenous cannabinoid system is an important regulatory system involved in physiological homeostasis. Endocannabinoid signaling is known to modulate neural development, immune function, metabolism, synaptic plasticity, and emotional state. Accumulating evidence also implicates brain endocannabinoid signaling in the processing of natural and drug-induced reward states and dysregulated endocannabinoid signaling in the etiology of aberrant reward function and drug addiction.


Cannabinoids and the Addictive Effects of Nicotine

L.V. Panlilio, S.R. Goldberg  (2017)

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Δ9-Tetrahydrocannabinol (THC) and nicotine are commonly used together in the form of cannabis and tobacco. Besides sharing similar routes of administration, these drugs affect reward-related brain circuits that partially overlap and interact. This interaction could be responsible for promoting addiction in co-users, but it might also provide new avenues for the treatment of addiction.


The endocannabinoid system: a new molecular target for the treatment of tobacco addiction

Maria Scherma, Paola Fadda, Bernard Le Foll, Benoit Forget, Walter Fratta, Steven R. Goldberg, and Gianluigi Tanda (November 2008)
This review will focus on the recently published literature about the role of the endocannabinoid system in nicotine addiction and on the endocannabinoid system as a novel molecular target for the discovery of medications for tobacco dependence.

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Important Notice

Leaving the CB1 Capital Management website to access a website hosted by a party unrelated to CB1 Capital Management. CB1 Capital Management assumes no responsibility for the accuracy of any of these studies nor does CB1 assume any obligation to update any of these studies based on subsequent research.

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Important Notice

Leaving the CB1 Capital Management website to access a website hosted by a party unrelated to CB1 Capital Management. CB1 Capital Management assumes no responsibility for the accuracy of any of these studies nor does CB1 assume any obligation to update any of these studies based on subsequent research.

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Important Notice

Leaving the CB1 Capital Management website to access a website hosted by a party unrelated to CB1 Capital Management. CB1 Capital Management assumes no responsibility for the accuracy of any of these studies nor does CB1 assume any obligation to update any of these studies based on subsequent research.

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Important Notice

Leaving the CB1 Capital Management website to access a website hosted by a party unrelated to CB1 Capital Management. CB1 Capital Management assumes no responsibility for the accuracy of any of these studies nor does CB1 assume any obligation to update any of these studies based on subsequent research.

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Important Notice

Leaving the CB1 Capital Management website to access a website hosted by a party unrelated to CB1 Capital Management. CB1 Capital Management assumes no responsibility for the accuracy of any of these studies nor does CB1 assume any obligation to update any of these studies based on subsequent research.

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Important Notice

Leaving the CB1 Capital Management website to access a website hosted by a party unrelated to CB1 Capital Management. CB1 Capital Management assumes no responsibility for the accuracy of any of these studies nor does CB1 assume any obligation to update any of these studies based on subsequent research.

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Important Notice

Leaving the CB1 Capital Management website to access a website hosted by a party unrelated to CB1 Capital Management. CB1 Capital Management assumes no responsibility for the accuracy of any of these studies nor does CB1 assume any obligation to update any of these studies based on subsequent research.

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Important Notice

Leaving the CB1 Capital Management website to access a website hosted by a party unrelated to CB1 Capital Management. CB1 Capital Management assumes no responsibility for the accuracy of any of these studies nor does CB1 assume any obligation to update any of these studies based on subsequent research.

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