Differences in basal and morphine-induced FosB/ΔFosB and pCREB immunoreactivities in dopaminergic brain regions of alcohol-preferring AA and alcohol-avoiding ANA rats

Kaste, Kristiina; Kivinummi, Tanja; Piepponen, Petteri; Kiianmaa, Kalervo; Ahtee, Liisa

doi:10.1016/j.pbb.2009.03.004

Cited by 12 publications

(9 citation statements)

References 43 publications

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“…Unexpectedly, we found that social interaction during extinction increased pCREB in the cingulate cortex area 1 (Cg1). In support of this finding, it has been shown that morphine increased pCREB expression in the prefrontal cortex of alcohol-avoiding rats in comparison with alcohol non-avoiding rats (Kaste et al, 2009). To date, not much data has been generated on the role of pCREB in the cingulate cortex area.…”

Section: Discussionmentioning

confidence: 74%

Preventive role of social interaction for cocaine conditioned place preference: correlation with FosB/DeltaFosB and pCREB expression in rat mesocorticolimbic areas

Rawas

Klement

Salti³

et al. 2012

Front. Behav. Neurosci.

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The worsening of drug abuse by drug-associated social interaction is a well-studied phenomenon. In contrast, the molecular mechanisms of the beneficial effect of social interaction, if offered as a mutually exclusive choice to drugs of abuse, are under-investigated. In a rat place preference conditioning (CPP) paradigm, four 15 min episodes of social interaction with a gender- and weight-matched male early-adult conspecific inhibited cocaine-induced reinstatement of cocaine CPP, a model of relapse. These protective effects of social interaction were paralleled by a reduced activation, as assessed by Zif268 expression, in brain areas known to play pivotal roles in drug-seeking behavior. Here we show that social interaction during extinction of cocaine CPP also reduced cocaine-CPP-stimulated FosB expression in the nucleus accumbens shell and core. In addition, social interaction during cocaine CPP extinction increased pCREB (cAMP response element binding protein) expression in the nucleus accumbens shell and the cingulate cortex area 1 (Cg1). Our results show that FosB and pCREB may be implicated in the protective effect of social interaction against cocaine-induced reinstatement of CPP. Thus, social interaction, if offered in a context that is clearly distinct from the previously drug-associated one, may profoundly inhibit relapse to cocaine addiction.

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Section: Discussionmentioning

confidence: 74%

Preventive role of social interaction for cocaine conditioned place preference: correlation with FosB/DeltaFosB and pCREB expression in rat mesocorticolimbic areas

Rawas

Klement

Salti³

et al. 2012

Front. Behav. Neurosci.

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“…Different chronic opiate administration paradigms activate FosB/ΔFosB in accumbal [20], [28], [29] and cortical [20] regions but the associated behavioral effects of morphine treatment were not linked to such changes. In our syudy of overexpression of ΔFosB did increase the rewarding and withdrawal properties of repeated morphine treatment [26].…”

Section: Introductionmentioning

confidence: 91%

Opiate Sensitization Induces FosB/ΔFosB Expression in Prefrontal Cortical, Striatal and Amygdala Brain Regions

et al. 2011

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Sensitization to the effects of drugs of abuse and associated stimuli contributes to drug craving, compulsive drug use, and relapse in addiction. Repeated opiate exposure produces behavioral sensitization that is hypothesized to result from neural plasticity in specific limbic, striatal and cortical systems. ΔFosB and FosB are members of the Fos family of transcription factors that are implicated in neural plasticity in addiction. This study examined the effects of intermittent morphine treatment, associated with motor sensitization, on FosB/ΔFosB levels using quantitative immunohistochemistry. Motor sensitization was tested in C57BL/6 mice that received six intermittent pre-treatments (on days 1, 3, 5, 8, 10, 12) with either subcutaneous morphine (10 mg/kg) or saline followed by a challenge injection of morphine or saline on day 16. Mice receiving repeated morphine injections demonstrated significant increases in locomotor activity on days 8, 10, and 12 of treatment (vs. day 1), consistent with development of locomotor sensitization. A morphine challenge on day 16 significantly increased locomotor activity of saline pre-treated mice and produced even larger increases in motor activity in the morphine pre-treated mice, consistent with the expression of opiate sensitization. Intermittent morphine pre-treatment on these six pre-treatment days produced a significant induction of FosB/ΔFosB, measured on day 16, in multiple brain regions including prelimbic (PL) and infralimbic (IL) cortex, nucleus accumbens (NAc) core, dorsomedial caudate-putamen (CPU), basolateral amygdala (BLA) and central nucleus of the amygdala (CNA) but not in a motor cortex control region. Opiate induced sensitization may develop via Fos/ΔFosB plasticity in motivational pathways (NAc), motor outputs (CPU), and associative learning (PL, IL, BLA) and stress pathways (CNA).

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“…Although it is well documented that chronic exposure to abused drugs including alcohol increases ΔFosB expression in several areas of the mesocorticolimbic system of rat brains (Atkins et al., 1999; Ehrlich et al., 2002; McDaid et al., 2006; Muller and Unterwald, 2005; Nye and Nestler, 1996; Perrotti et al., 2008, 2008; Pich et al., 1997; Zachariou et al., 2006), it still remains unknown whether chronic voluntary alcohol consumption can alter ΔFosB. Even though it has been shown previously that the opioid receptor antagonist naltrexone significantly reduces alcohol consumption in many studies in human and experimental animals (Bienkowski et al., 1999; Cichelli and Lewis, 2002; Coonfield et al., 2004; O’Malley et al., 2002; Stromberg, 2004; Zalewska‐Kaszubska et al., 2008), study on the possible participation of opioid receptors in ΔFosB accumulation associated with drugs of abuse is lacking (Kaste et al., 2009; Marttila et al., 2007). Therefore, we conducted this study to determine: (i) whether chronic voluntary alcohol consumption can alter FosB/ΔFosB and (ii) whether naltrexone‐induced reduction of alcohol consumption is associated with changes in FosB/ΔFosB.…”

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confidence: 99%

Region‐Specific Induction of FosB/ΔFosB by Voluntary Alcohol Intake: Effects of Naltrexone

Li¹,

Cheng²,

Bian³

et al. 2010

Alcoholism Clin & Exp Res

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Background ΔFosB is the best characterized transcription factor induced by chronic stimulation. Although previous studies have demonstrated that chronic passive ethanol exposure alters ΔFosB immunoreactivity (IR), the effect of chronic voluntary ethanol consumption on ΔFosB remains unknown. Furthermore, although previous studies have demonstrated that the opioid antagonist naltrexone reduces alcohol consumption in clinical and pre-clinical settings, the effect of naltrexone on FosB/ΔFosB has not been explored. Here we examined the effects of chronic voluntary ethanol intake and naltrexone on FosB/ΔFosB IR in striatal region and prefrontal cortex, and the effect of naltrexone on voluntary ethanol intake. Methods We utilized immunohistochemistry to define the changes in FosB/ΔFosB IR induced by chronic voluntary ethanol intake under a two-bottle intermittent access of 20% ethanol model and by systematic administration (intraperitoneal injection) of naltrexone in Sprague-Dawley rats. Results Chronic (15 drinking sessions in 35 days) voluntary ethanol intake robustly induces FosB/ΔFosB IR in nucleus accumbens core, dorsolateral striatum and orbitofrontal cortex, but not in nucleus accumbens shell, dorsomedial striatum and medial prefrontal cortex. Systemic administration of naltrexone for six days significantly reduced voluntary ethanol consumption and FosB/ΔFosB IR induced by chronic voluntary ethanol intake. Conclusion Our results suggest that chronic voluntary ethanol intake induces FosB/ΔFosB IR in a sub-region-specific manner and which involves activation of endogenous opioid system.

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Differences in basal and morphine-induced FosB/ΔFosB and pCREB immunoreactivities in dopaminergic brain regions of alcohol-preferring AA and alcohol-avoiding ANA rats

Cited by 12 publications

References 43 publications

Preventive role of social interaction for cocaine conditioned place preference: correlation with FosB/DeltaFosB and pCREB expression in rat mesocorticolimbic areas

Preventive role of social interaction for cocaine conditioned place preference: correlation with FosB/DeltaFosB and pCREB expression in rat mesocorticolimbic areas

Opiate Sensitization Induces FosB/ΔFosB Expression in Prefrontal Cortical, Striatal and Amygdala Brain Regions

Region‐Specific Induction of FosB/ΔFosB by Voluntary Alcohol Intake: Effects of Naltrexone

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