Blockade of Cue‐induced Brain Activation of Abstinent Alcoholics by a Single Administration of Amisulpride as Measured With fMRI

Hermann, Derik; Smolka, Michael N.; Wrase, Jana; Klein, Sabine; Nikitopoulos, J.; Georgi, Alexander; Braus, Dieter F.; Flor, Herta; Mann, Karl; Heinz, Andreas

doi:10.1111/j.1530-0277.2006.00174.x

Cited by 89 publications

(56 citation statements)

References 33 publications

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“…In the present study, a priori ROI analyses indicated that gustatory alcohol cues elicited activation in many of the structures that have been previously implicated in the development and expression of craving for a variety of drugs of abuse including the VTA/SN (Kareken et al, 2004), OFC (Hermann et al, 2006;Myrick et al, 2004), and medial PFC (Kalivas and Volkow, 2005;Myrick et al, 2004;Park et al, in press). Interestingly, we did not observe differential activity in the VS corresponding to alcohol vs control cues as previously reported by other groups (eg Kareken et al, 2004); instead, we found increased DS/caudate activity.…”

Section: Discussionmentioning

confidence: 94%

Exposure to the Taste of Alcohol Elicits Activation of the Mesocorticolimbic Neurocircuitry

Filbey

Claus

Audette

et al. 2007

Neuropsychopharmacol

250

216

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A growing number of imaging studies suggest that alcohol cues, mainly visual, elicit activation in mesocorticolimbic structures. Such findings are consistent with the growing recognition that these structures play an important role in the attribution of incentive salience and the pathophysiology of addiction. The present study investigated whether the presentation of alcohol taste cues can activate brain regions putatively involved in the acquisition and expression of incentive salience. Using functional magnetic resonance imaging, we recorded BOLD activity while delivering alcoholic tastes to 37 heavy drinking but otherwise healthy volunteers. The results yielded a pattern of BOLD activity in mesocorticolimbic structures (ie prefrontal cortex, striatum, ventral tegmental area/substantia nigra) relative to an appetitive control. Further analyses suggested strong connectivity between these structures during cue-elicited urge and demonstrated significant positive correlations with a measure of alcohol use problems (ie the Alcohol Use Disorders Identification Test). Thus, repeated exposure to the taste alcohol in the scanner elicits activation in mesocorticolimbic structures, and this activation is related to measures of urge and severity of alcohol problems.

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Section: Discussionmentioning

confidence: 94%

Exposure to the Taste of Alcohol Elicits Activation of the Mesocorticolimbic Neurocircuitry

Filbey

Claus

Audette

et al. 2007

Neuropsychopharmacol

250

216

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“…This activation enhances neural excitability and excitatory synaptic activity within dHipp (Hopkins and Johnston, 1984;Pedarzani and Storm, 1993) and PL-mPFC (Ji et al, 2008;Otis et al, 2013). Thus, these structures become active following drug-associated cue exposure (Hearing et al, 2010;Hermann et al, 2006;Miller and Marshall, 2004;Neiswander et al, 2000), leading to memory retrieval. Inhibiting dHipp or PL-mPFC activation by blocking b-AR activity likely renders cocaine-conditioned cues less salient, preventing drug-associated memory retrieval.…”

Section: Discussionmentioning

confidence: 99%

“…Moreover, norepinephrine (NE) and b-AR activation within dHipp are critical for contextual fear memory retrieval, but not for fear expression alone (Murchison et al, 2004). The dHipp is activated by drug-associated cue exposure in both rodents (Neisewander et al, 2000;Hearing et al, 2010) and humans (Hermann et al, 2006), and dHipp inactivation prevents context-driven drug seeking and reinstatement (Fuchs et al, 2005;Meyers et al, 2006). Despite evidence that dHipp is involved in memory retrieval and reinstatement, it remains unclear whether dHipp b-AR activation is required for drug-associated memory retrieval and subsequent druginduced reinstatement.…”

Section: Introductionmentioning

confidence: 99%

Inhibition of Hippocampal β-Adrenergic Receptors Impairs Retrieval But Not Reconsolidation of Cocaine-Associated Memory and Prevents Subsequent Reinstatement

Otis

Fitzgerald

Mueller

2013

Neuropsychopharmacol

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Retrieval of drug-associated memories is critical for maintaining addictive behaviors, as presentation of drug-associated cues can elicit drug seeking and relapse. Recently, we and others have demonstrated that b-adrenergic receptor (b-AR) activation is necessary for retrieval using both rat and human memory models. Importantly, blocking retrieval with b-AR antagonists persistently impairs retrieval and provides protection against subsequent reinstatement. However, the neural locus at which b-ARs are required for maintaining retrieval and subsequent reinstatement is unclear. Here, we investigated the necessity of dorsal hippocampus (dHipp) b-ARs for drugassociated memory retrieval. Using a cocaine conditioned place preference (CPP) model, we demonstrate that local dHipp b-AR blockade before a CPP test prevents CPP expression shortly and long after treatment, indicating that dHipp b-AR blockade induces a memory retrieval disruption. Furthermore, this retrieval disruption provides long-lasting protection against cocaine-induced reinstatement. The effects of b-AR blockade were dependent on memory reactivation and were not attributable to reconsolidation disruption as blockade of b-ARs immediately after a CPP test had little effect on subsequent CPP expression. Thus, cocaine-associated memory retrieval is mediated by b-AR activity within the dHipp, and disruption of this activity could prevent cue-induced drug seeking and relapse long after treatment.

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“…Other reward-related areas, including the insula (29)(30)(31) and cingulate gyrus (8,14,15,29,(32)(33)(34)(35)(36), show increased activity with the presentation of drug-related stimuli. Presentation of these stimuli is also associated with increased activity in brain structures that underlie reward and emotion regulation, such as the thalamus (9,30,(37)(38)(39)(40) and amygdala (32,39).…”

mentioning

confidence: 99%

Marijuana craving in the brain

Filbey

Schacht

Myers

et al. 2009

Proc. Natl. Acad. Sci. U.S.A.

237

191

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Craving is one of the primary behavioral components of drug addiction, and cue-elicited craving is an especially powerful form of this construct. While cue-elicited craving and its underlying neurobiological mechanisms have been extensively studied with respect to alcohol and other drugs of abuse, the same cannot be said for marijuana. Cue-elicited craving for other drugs of abuse is associated with increased activity in a number of brain areas, particularly the reward pathway. This study used functional magnetic resonance imaging (fMRI) to examine cue-elicited craving for marijuana. Thirty-eight regular marijuana users abstained from use for 72 h and were presented with tactile marijuana-related and neutral cues while undergoing a fMRI scan. Several structures in the reward pathway, including the ventral tegmental area, thalamus, anterior cingulate, insula, and amygdala, demonstrated greater blood oxygen level dependent (BOLD) activation in response to the marijuana cue as compared with the neutral cue. These regions underlie motivated behavior and the attribution of incentive salience. Activation of the orbitofrontal cortex and nucleus accumbens was also positively correlated with problems related to marijuana use, such that greater BOLD activation was associated with greater number of items on a marijuana problem scale. Thus, cue-elicited craving for marijuana activates the reward neurocircuitry associated with the neuropathology of addiction, and the magnitude of activation of these structures is associated with severity of cannabis-related problems. These findings may inform the development of treatment strategies for cannabis dependence.cannabis ͉ cue ͉ fMRI ͉ reward

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Blockade of Cue‐induced Brain Activation of Abstinent Alcoholics by a Single Administration of Amisulpride as Measured With fMRI

Abstract: Amisulpride medication was associated with reduced cue-induced activation of the thalamus, a brain region closely connected with frontostriatal circuits that regulate behavior and may influence relapse risk.

Cited by 89 publications

References 33 publications

Exposure to the Taste of Alcohol Elicits Activation of the Mesocorticolimbic Neurocircuitry

Exposure to the Taste of Alcohol Elicits Activation of the Mesocorticolimbic Neurocircuitry

Inhibition of Hippocampal β-Adrenergic Receptors Impairs Retrieval But Not Reconsolidation of Cocaine-Associated Memory and Prevents Subsequent Reinstatement

Marijuana craving in the brain

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