Ethanol alters the effect of kappa receptor ligands on dopamine release in the nucleus accumbens

Lindholm, Sara; Rosin, Åsa; Dahlin, Ingrid; Georgieva, Jeanette; Franck, Johan

doi:10.1016/j.physbeh.2007.05.039

Cited by 40 publications

(35 citation statements)

References 22 publications

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“…As with other drugs of abuse, ethanol acutely induces dopamine release in NAcc (Weiss et al, 1993;Gonzales et al, 2004), whereas stimulation of KORs reduces the release of dopamine in NAcc (Spanagel et al, 1992). Ethanol-dependent rats show increased dopamine release when intoxicated but reduced basal dopamine tone during withdrawal, which is increased by KOR antagonism (Diana et al, 1993;Lindholm et al, 2007). Consistent with this, KOR knockout mice showed elevated ethanolevoked dopamine release in the NAcc (Zapata and Shippenberg, 2006).…”

Section: Introductionmentioning

confidence: 78%

“…KORs are localized on axon terminals as well as on neuronal cell bodies, and they may act through two mechanisms: by inhibition of neurotransmission directly at terminal release sites (Svingos et al, 1999;Li et al, 2012) as well as by direct hyperpolarization of cell bodies (Margolis et al, 2003). An example of such modulation of neurotransmission, a decrease in dopamine release by the dynorphin/ KOR system in the nucleus accumbens (NAcc), was proposed as one mechanism underlying the effect on alcohol consumption (Lindholm et al, 2007). As with other drugs of abuse, ethanol acutely induces dopamine release in NAcc (Weiss et al, 1993;Gonzales et al, 2004), whereas stimulation of KORs reduces the release of dopamine in NAcc (Spanagel et al, 1992).…”

Section: Introductionmentioning

confidence: 99%

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κ-Opioid Receptors in the Central Amygdala Regulate Ethanol Actions at Presynaptic GABAergic Sites

Kang-Park

Kieffer

Roberts

et al. 2013

J Pharmacol Exp Ther

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Section: Introductionmentioning

confidence: 78%

Section: Introductionmentioning

confidence: 99%

κ-Opioid Receptors in the Central Amygdala Regulate Ethanol Actions at Presynaptic GABAergic Sites

Kang-Park

Kieffer

Roberts

et al. 2013

J Pharmacol Exp Ther

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“…Ascending projections from the CeA innervate nuclei important for signaling biologically relevant information to promote survival (Berthoud, 2002), such as the ventral striatum, among others. The dense projection from the CeA to the bed nucleus of the stria terminalis, in concert with the ventral striatum, integrates emotional and motivational information and is recruited in dependence to promote excessive alcohol seeking and consumption (Koob, 2009), and KORs have been shown to modulate the function of all primary extended amygdala nuclei (Lindholm et al, 2007;Li et al, 2012;Kallupi et al, 2013). From a functional circuitry-based perspective, an important question for future research to assess would be the net effect of nor-BNI on CeA activity and output to different cortical, limbic, and brainstem nuclei.…”

Section: Discussionmentioning

confidence: 99%

Dissociating Motivational From Physiological Withdrawal in Alcohol Dependence: Role of Central Amygdala κ-Opioid Receptors

Kissler

Walker

2015

Neuropsychopharmacol

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Chronic intermittent alcohol vapor exposure leads to increased dynorphin (DYN) A-like peptide expression and heightened kappa-opioid receptor (KOR) signaling in the central nucleus of the amygdala (CeA) and these neuroadaptive responses differentiate alcohol-dependent from non-dependent phenotypes. Important for therapeutic development efforts is understanding the nature of the stimulus that drives dependence-like phenotypes such as escalated alcohol self-administration. Accordingly, the present study examined the impact of intraCeA KOR antagonism on escalated operant alcohol self-administration and physiological withdrawal symptoms during acute withdrawal and protracted abstinence in rats previously exposed to chronic intermittent alcohol vapor. Following operant training, rats were implanted with intra-CeA guide cannula and exposed to long-term intermittent alcohol vapor exposure that resulted in escalated alcohol selfadministration and elevated physiological withdrawal signs during acute withdrawal. Animals received intra-CeA infusions of the KOR antagonist nor-binaltorphimine (nor-BNI; 0, 2, 4, or 6 μg) prior to operant alcohol self-administration sessions and physiological withdrawal assessment during acute withdrawal and protracted abstinence. The results indicated that site-specific KOR antagonism in the CeA ameliorated escalated alcohol self-administration during both acute withdrawal and protracted abstinence test sessions, whereas KOR antagonism had no effect on physiological withdrawal scores at either time point. These results dissociate escalated alcohol selfadministration from physiological withdrawal symptoms in relation to KOR signaling in the CeA and help clarify the nature of the stimulus that drives escalated alcohol self-administration during acute withdrawal and protracted abstinence.

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“…Ten minutes U50,488 pretreatment prior to ethanol decreases ethanol-induced CPP using conditioning procedures under which U50,488 does not produce CPA suggesting U50,488 decreases the conditioned effects of ethanol independently of its aversive effects. Lindholm et al [363] demonstrated that tonic inhibition of DA overflow by KORs in the NAcc is enhanced after repeated injections of moderate doses of ethanol, which may contribute to decreased motivation and negative affect after repeated ethanol exposure. Findings regarding the effects of KOR ligands on ethanol self-administration are discrepant.…”

Section: Ethanolmentioning

confidence: 99%

The dynorphin/κ-opioid receptor system and its role in psychiatric disorders

Tejeda

Shippenberg

Henriksson

2011

Cell. Mol. Life Sci.

145

144

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The dynorphin/κ-opioid receptor system has been implicated in the pathogenesis and pathophysiology of several psychiatric disorders. In the present review, we present evidence indicating a key role for this system in modulating neurotransmission in brain circuits that subserve mood, motivation, and cognitive function. We overview the pharmacology, signaling, post-translational, post-transcriptional, transcriptional, epigenetic and cis regulation of the dynorphin/κ-opioid receptor system, and critically review functional neuroanatomical, neurochemical, and pharmacological evidence, suggesting that alterations in this system may contribute to affective disorders, drug addiction, and schizophrenia. We also overview the dynorphin/κ-opioid receptor system in the genetics of psychiatric disorders and discuss implications of the reviewed material for therapeutics development.

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Ethanol alters the effect of kappa receptor ligands on dopamine release in the nucleus accumbens

Cited by 40 publications

References 22 publications

κ-Opioid Receptors in the Central Amygdala Regulate Ethanol Actions at Presynaptic GABAergic Sites

κ-Opioid Receptors in the Central Amygdala Regulate Ethanol Actions at Presynaptic GABAergic Sites

Dissociating Motivational From Physiological Withdrawal in Alcohol Dependence: Role of Central Amygdala κ-Opioid Receptors

The dynorphin/κ-opioid receptor system and its role in psychiatric disorders

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