Clinical Neuroscience of Addiction: Similarities and Differences Between Alcohol and Other Drugs

Karoly, Hollis C.; YorkWilliams, Sophie L.; Hutchison, Kent E.

doi:10.1111/acer.12884

Cited by 16 publications

(15 citation statements)

References 166 publications

(315 reference statements)

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“…Although CB 1 -CB 2 heteromers have not been evidenced in the cortex so far, one can postulate that cocaine could prevent their neuroprotective effect by decreasing their expression, which may contribute to the addiction vulnerability observed in adolescents (Bagot et al, 2015). CB 1 -CB 2 heteromers may therefore represent a therapeutic target to reduce neuroinflammation that develops in SUD (Karoly et al, 2015).…”

Section: Cannabinoid Cb 1 -Cb 2 Heteromersmentioning

confidence: 99%

G protein-coupled receptor heteromers are key players in substance use disorder

Derouiche

Massotte

2019

Neuroscience & Biobehavioral Reviews

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G protein-coupled receptors (GPCR) represent the largest family of membrane proteins in the human genome. Physical association between two different GPCRs is linked to functional interactions which generates a novel entity, called heteromer, with specific ligand binding and signaling properties. Heteromerization is increasingly recognized to take place in the mesocorticolimbic pathway and to contribute to various aspects related to substance use disorder. This review focuses on heteromers identified in brain areas relevant to drug addiction. We report changes at the molecular and cellular levels that establish specific functional impact and highlight behavioral outcome in preclinical models. Finally, we briefly discuss selective targeting of native heteromers as an innovative therapeutic option.

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Section: Cannabinoid Cb 1 -Cb 2 Heteromersmentioning

confidence: 99%

G protein-coupled receptor heteromers are key players in substance use disorder

Derouiche

Massotte

2019

Neuroscience & Biobehavioral Reviews

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“…Although the general idea of applying non-invasive brain stimulation to treat SUD symptoms is not new [ 9 , 11 , 27 , 31 , 32 ], the mechanism of action of these methods, including DTMS, is still unclear. Past reviews have shown that the high-frequency rTMS with F8-coil is able to transiently reduce craving for various substances [ 9 , 14 , 32 – 35 ], possibly due to changes in the dopamine and glutamate activity in the cortico-striato-limbic systems implicated in SUD [ 9 , 14 , 15 ]. These changes may include increased dopaminergic release and/or improved dopaminergic binding in the striatum, although multiple networks and neurotransmitter systems are likely to be involved depending on the type of SUD [ 36 ].…”

Section: Discussionmentioning

confidence: 99%

“…These changes may include increased dopaminergic release and/or improved dopaminergic binding in the striatum, although multiple networks and neurotransmitter systems are likely to be involved depending on the type of SUD [ 36 ]. In general, although various SUD affect common neural pathways, share common molecular targets, and have similar reinforcing effects, they may access the reward system via different mechanisms [ 15 ]. Advancing efficient translational research is required to find new pharmacological treatments for SUD [ 15 ].…”

Section: Discussionmentioning

confidence: 99%

“…In general, although various SUD affect common neural pathways, share common molecular targets, and have similar reinforcing effects, they may access the reward system via different mechanisms [ 15 ]. Advancing efficient translational research is required to find new pharmacological treatments for SUD [ 15 ]. The non-invasive brain stimulation could be a viable alternative to pharmacotherapy in the short-term and/or could offer a longer-term relief from SUD although it may require some individualization of protocols and/or stimulation sites rather than the ‘one-size-fits-all’ approach [ 11 ].…”

Section: Discussionmentioning

confidence: 99%

“…Such a broad stimulation with H-coils could increase the electrical field in deeper, subcortical brain regions [ 12 , 13 ]. Therefore, DTMS with H-coils is a promising candidate for treatment of various SUD that affect similar neural circuitry (deeper cortico-striatal pathways) [ 14 ] and share numerous molecular targets [ 15 ].…”

Section: Introductionmentioning

confidence: 99%

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Can deep transcranial magnetic stimulation (DTMS) be used to treat substance use disorders (SUD)? A systematic review

2018

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BackgroundDeep transcranial magnetic stimulation (DTMS) is a non-invasive method of stimulating widespread cortical areas and, presumably, deeper neural networks. The current study assessed the effects of DTMS in the treatment of substance use disorders (SUD) using a systematic review.MethodsElectronic literature search (PsycInfo, Medline until April 2017) identified k = 9 studies (k = 4 randomized-controlled trials, RCTs, with inactive sham and k = 5 open-label studies). DTMS was most commonly applied using high frequency/intensity (10–20 Hz/100–120% of the resting motor threshold, MT) protocols for 10–20 daily sessions in cases with alcohol, nicotine or cocaine use disorders. The outcome measures were craving and dependence (according to standardized scales) or consumption (frequency, abstinence or results of biological assays) at the end of the daily treatment phases and at the last follow-up.ResultsAcute and longer-term (6–12 months) reductions in alcohol craving were observed after 20 sessions (20 Hz, 120% MT) relative to baseline in k = 4 open-label studies with comorbid SUD and major depressive disorder (MDD). In k = 2 RCTs without MDD, alcohol consumption acutely decreased after 10–12 sessions (10–20 Hz, 100–120% MT) relative to baseline or to sham. Alcohol craving was reduced only after higher frequency/intensity DTMS (20 Hz, 120% MT) relative to sham in k = 1 RCT. Nicotine consumption was reduced and abstinence was increased after 13 sessions (10 Hz, 120% MT) and at the 6-month follow-up relative to sham in k = 1 RCT. Cocaine craving was reduced after 12 sessions (15 Hz, 100% MT) and at the 2-month follow-up relative to baseline in k = 1 open-label study while consumption was reduced after 12 sessions (10 Hz, 100% MT) relative to baseline but not to sham in k = 1 RCT.ConclusionsHigh-frequency DTMS may be effective at treating some SUD both acutely and in the longer-term. Large RCTs with inactive sham are required to determine the efficacy and the optimal stimulation parameters of DTMS for the treatment of SUD.

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Do Alcohol-Related AMPA-Type Glutamate Receptor Adaptations Promote Intake?

Hopf

Mangieri

2018

The Neuropharmacology of Alcohol

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Ionotropic glutamate receptors (AMPA, NMDA, and kainate receptors) play a central role in excitatory glutamatergic signaling throughout the brain. As a result, functional changes, especially long-lasting forms of plasticity, have the potential to profoundly alter neuronal function and the expression of adaptive and pathological behaviors. Thus, alcohol-related adaptations in ionotropic glutamate receptors are of great interest, since they could promote excessive alcohol consumption, even after long-term abstinence. Alcohol- and drug-related adaptations in NMDARs have been recently reviewed, while less is known about kainate receptor adaptations. Thus, we focus here on functional changes in AMPARs, tetramers composed of GluA1-4 subunits. Long-lasting increases or decreases in AMPAR function, the so-called long-term potentiation or depression, have widely been considered to contribute to normal and pathological memory states. In addition, a great deal has been learned about the acute regulation of AMPARs by signaling pathways, scaffolding and auxiliary proteins, intracellular trafficking, and other mechanisms. One important common adaptation is a shift in AMPAR subunit composition from GluA2-containing, calcium-impermeable AMPARs (CIARs) to GluA2-lacking, calcium-permeable AMPARs (CPARs), which is observed under a broad range of conditions including intoxicant exposure or intake, stress, novelty, food deprivation, and ischemia. This shift has the potential to facilitate AMPAR currents, since CPARs have much greater single-channel currents than CIARs, as well as faster AMPAR activation kinetics (although with faster inactivation) and calcium-related activity. Many tools have been developed to interrogate particular aspects of AMPAR signaling, including compounds that selectively inhibit CPARs, raising exciting translational possibilities. In addition, recent studies have used transgenic animals and/or optogenetics to identify AMPAR adaptations in particular cell types and glutamatergic projections, which will provide critical information about the specific circuits that CPARs act within. Also, less is known about the specific nature of alcohol-related AMPAR adaptations, and thus we use other examples that illustrate more fully how particular AMPAR changes might influence intoxicant-related behavior. Thus, by identifying alcohol-related AMPAR adaptations, the specific molecular events that underlie them, and the cells and projections in which they occur, we hope to better inform the development of new therapeutic interventions for addiction.

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Clinical Neuroscience of Addiction: Similarities and Differences Between Alcohol and Other Drugs

Cited by 16 publications

References 166 publications

G protein-coupled receptor heteromers are key players in substance use disorder

G protein-coupled receptor heteromers are key players in substance use disorder

Can deep transcranial magnetic stimulation (DTMS) be used to treat substance use disorders (SUD)? A systematic review

Do Alcohol-Related AMPA-Type Glutamate Receptor Adaptations Promote Intake?

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