Lesions of the Extended Amygdala in C57BL/6J Mice Do Not Block the Intermittent Ethanol Vapor‐Induced Increase in Ethanol Consumption

Dhaher, Ronnie; Finn, Deborah A.; Snelling, Christopher; Hitzemann, Robert

doi:10.1111/j.1530-0277.2007.00566.x

Cited by 64 publications

(67 citation statements)

References 34 publications

(47 reference statements)

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“…This level of increased ethanol consumption attained in the present series of experiments has been previously shown to result in significant elevation (two-to threefold increase) in blood ethanol levels and brain ethanol concentrations (Griffin et al, 2009b). These results (increased alcohol consumption) are congruent with those reported by others using similar procedures in mice (Finn et al, 2007;Dhaher et al, 2008) and rats (Gehlert et al, 2007;Roberts et al, 1996;Roberts et al, 2000;Sommer et al, 2008).…”

Section: Discussionsupporting

confidence: 82%

Increased Extracellular Glutamate In the Nucleus Accumbens Promotes Excessive Ethanol Drinking in Ethanol Dependent Mice

Griffin

Haun

Hazelbaker

et al. 2013

Neuropsychopharmacol

127

112

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Using a well-established model of ethanol dependence and relapse, this study examined adaptations in glutamatergic transmission in the nucleus accumbens (NAc) and their role in regulating voluntary ethanol drinking. Mice were first trained to drink ethanol in a free-choice, limited access (2 h/day) paradigm. One group (EtOH mice) received repeated weekly cycles of chronic intermittent ethanol (CIE) exposure with intervening weeks of test drinking sessions, whereas the remaining mice (CTL mice) were similarly treated but did not receive CIE treatment. Over repeated cycles of CIE exposure, EtOH mice exhibited significant escalation in drinking (up to B3.5 g/kg), whereas drinking remained relatively stable at baseline levels (2-2.5 g/kg) in CTL mice. Using in vivo microdialysis procedures, extracellular glutamate (GLU EX ) levels in the NAc were increased approximately twofold in EtOH mice compared with CTL mice, and this difference was observed 7 days after final CIE exposure, indicating that this hyperglutamatergic state persisted beyond acute withdrawal. This finding prompted additional studies examining the effects of pharmacologically manipulating GLU EX in the NAc on ethanol drinking in the CIE model. The non-selective glutamate reuptake antagonist, threo-b-benzyloxyaspartate (TBOA), was bilaterally microinjected into the NAc and found to dose-dependently increase drinking in nondependent (CTL) mice to levels attained by dependent (EtOH) mice. TBOA also further increased drinking in EtOH mice. In contrast, reducing glutamatergic transmission in the NAc via bilateral injections of the metabotropic glutamate receptor-2/3 agonist LY379268 reduced drinking in dependent (EtOH) mice to nondependent (CTL) levels, whereas having a more modest effect in decreasing ethanol consumption in CTL mice. Taken together, these data support an important role of glutamatergic transmission in the NAc in regulating ethanol drinking. Additionally, these results indicate that ethanol dependence produces adaptations that favor elevated glutamate activity in the NAc which, in turn, promote excessive levels of ethanol consumption associated with dependence.

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Section: Discussionsupporting

confidence: 82%

Increased Extracellular Glutamate In the Nucleus Accumbens Promotes Excessive Ethanol Drinking in Ethanol Dependent Mice

Griffin

Haun

Hazelbaker

et al. 2013

Neuropsychopharmacol

127

112

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“…Moreover, a study identified the putamen as a significant region in the representation of action-specific values that are important for the mediation between reward and adaptive behavior (FitzGerald, Friston, & Dolan, 2012), linking reward to action (Redgrave et al, 2010), planning actions (Monchi, Ko, & Strafella, 2006), and encoding habits as opposed to goal-directed values (Wunderlich, Dayan, & Dolan, 2012) e processes that are crucial for the transition to alcohol addiction and its maintenance. The activation of the putamen was also suggested to be associated with alcohol craving (Heinz et al, 2005) and alcohol preference, via projections from the amygdala (Dhaher, Finn, Snelling, & Hitzemann, 2008;Russchen & Price, 1984). BDNF Val66Met might thus have an effect on neural correlates of processing rewarding outcomes and might in consequence modulate adaptive behavior in a rewarding context, which might turn into increased habitual problematic alcohol consumption and thus could result in increased alcohol craving and manifest as alcohol addiction.…”

Section: Discussionmentioning

confidence: 96%

BDNF Val66Met and reward-related brain function in adolescents: role for early alcohol consumption

Nees

Witt

Dinu-Biringer

et al. 2015

Alcohol

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“…The regions compared (nucleus accumbens shell [SH], central nucleus of the amygdala [CeA], and prelimbic cortex [PL]) are components of the addiction circuit (Koob and Volkow, 2010, 2016). A previous study (Dhaher et al, 2008) suggested that the CeA but not the SH has a more significant role in preference (2-bottle choice) consumption. The short-term selection of the High and Low ethanol preference lines from heterogeneous stock-collaborative cross (HS-CC) founders has been described elsewhere (Colville et al, 2017).…”

Section: Introductionmentioning

confidence: 92%

Regional Differences and Similarities in the Brain Transcriptome for Mice Selected for Ethanol Preference From HS-CC Founders

et al. 2018

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The high genetic complexity found in heterogeneous stock (HS-CC) mice, together with selective breeding, can be used to detect new pathways and mechanisms associated with ethanol preference and excessive ethanol consumption. We predicted that these pathways would provide new targets for therapeutic manipulation. Previously (Colville et al., 2017), we observed that preference selection strongly affected the accumbens shell (SH) genes associated with synaptic function and in particular genes associated with synaptic tethering. Here we expand our analyses to include substantially larger sample sizes and samples from two additional components of the “addiction circuit,” the central nucleus of the amygdala (CeA) and the prelimbic cortex (PL). At the level of differential expression (DE), the majority of affected genes are region-specific; only in the CeA did the DE genes show a significant enrichment in GO annotation categories, e.g., neuron part. In all three brain regions the differentially variable genes were significantly enriched in a single network module characterized by genes associated with cell-to-cell signaling. The data point to glutamate plasticity as being a key feature of selection for ethanol preference. In this context the expression of Dlg2 which encodes for PSD-93 appears to have a key role. It was also observed that the expression of the clustered protocadherins was strongly associated with preference selection.

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Lesions of the Extended Amygdala in C57BL/6J Mice Do Not Block the Intermittent Ethanol Vapor‐Induced Increase in Ethanol Consumption

Cited by 64 publications

References 34 publications

Increased Extracellular Glutamate In the Nucleus Accumbens Promotes Excessive Ethanol Drinking in Ethanol Dependent Mice

Increased Extracellular Glutamate In the Nucleus Accumbens Promotes Excessive Ethanol Drinking in Ethanol Dependent Mice

BDNF Val66Met and reward-related brain function in adolescents: role for early alcohol consumption

Regional Differences and Similarities in the Brain Transcriptome for Mice Selected for Ethanol Preference From HS-CC Founders

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