Effects of acute and repeated administration of salvinorin A on dopamine function in the rat dorsal striatum

Gehrke, Brenda J.; Chefer, Vladimir I.; Shippenberg, Toni S.

doi:10.1007/s00213-007-1067-6

Cited by 63 publications

(74 citation statements)

References 31 publications

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“…The maximum CPP response observed with the 40 g/kg dose was reduced by the CB 1 receptor inverse-agonist rimonabant as well as norBNI. In contrast to other studies (Zhang et al, 2005;Gehrke et al, 2008), 40 g/kg salvinorin A increased extracellular DA by ϳ150% of baseline for 140 min in the shell of the nucleus accumbens. Consistent with the salvinorin A-induced increase in extracellular DA observed in this study, intracerebroventricular salvinorin A supported self-administration behavior, an effect that was attenuated by either rimonabant or norBNI.…”

Section: Studies Examining Stress Mood and Rewardcontrasting

confidence: 95%

“…decreased extracellular DA but not 5-HT. Gehrke et al, (2008) extended these findings. This study showed that administration of salvinorin A (1.0 and 3.2 mg/kg i.p.)…”

Section: Studies Examining Stress Mood and Rewardmentioning

confidence: 53%

“…Some of these were described above and will not be elaborated upon here (Beerepoot et al, 2008;Braida et al, 2008Braida et al, , 2009Gehrke et al, 2008). In vitro studies demonstrated differential effects of salvinorin A and standard KOP agonists.…”

Section: Studies Examining Stress Mood and Rewardmentioning

confidence: 99%

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Neuropharmacology of the Naturally Occurring κ-Opioid Hallucinogen Salvinorin A

2011

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Section: Studies Examining Stress Mood and Rewardcontrasting

confidence: 95%

“…decreased extracellular DA but not 5-HT. Gehrke et al, (2008) extended these findings. This study showed that administration of salvinorin A (1.0 and 3.2 mg/kg i.p.)…”

Section: Studies Examining Stress Mood and Rewardmentioning

confidence: 53%

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Neuropharmacology of the Naturally Occurring κ-Opioid Hallucinogen Salvinorin A

2011

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“…Also, κ-agonists attenuate the development and long-term expression of cocaine-induced behavioral sensitization following their repeated, intermittent administration [91] . These effects most likely result from the inhibition of limbic DA release after acute administration of κ-agonists [34,88,92,93] . However, there is paradoxical evidence that continuous or prior exposure to κ-agonists can potentiate the rewarding effects of cocaine under stress conditions and stress-induced reinstatement [36,94,95] .…”

Section: Potential Therapeutic Applications Of κ-Opioid Agonists In Pmentioning

confidence: 99%

The role of κ-opioid receptor activation in mediating antinociception and addiction

et al. 2010

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The κ-opioid receptor (KOR), a member of the opioid receptor family, is widely expressed in the central nervous system and peripheral tissues. Substantial evidence has shown that activation of KOR by agonists and endogenous opioid peptides in vivo may produce a strong analgesic effect that is free from the abuse potential and the adverse side effects of µ-opioid receptor (MOR) agonists, such as morphine. In addition, activation of the KOR has also been shown to exert an inverse effect on morphine-induced adverse actions, such as tolerance, reward, and impairment of learning and memory. Therefore, the KOR has received much attention in the effort to develop alternative analgesics to MOR agonists and agents for the treatment of drug addiction. However, KOR agonists also produce several severe undesirable side effects such as dysphoria, water diuresis, salivation, emesis, and sedation in nonhuman primates, which may limit the clinical utility of KOR agonists for pain and drug abuse treatment. This article will review the role of KOR activation in mediating antinociception and addiction. The possible therapeutic application of κ-agonists in the treatment of pain and drug addiction is also discussed.

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“…These receptors not only have traditional G i/o -negative regulatory effects on adenylate cyclase activity but also couple to mitogen-activated protein kinase pathways and inward rectifying potassium channels (Bruchas et al, 2010;Al-Hasani and Bruchas, 2011). Although the mechanisms of stress-induced reinstatement of drug seeking and drug reward are complex, it has been shown that stress causes dynorphin release and KOR activation within both dopaminergic and serotonergic nuclei (Carlezon et al, 2006;Ebner et al, 2010;Gehrke et al, 2008;Land et al, 2008;Zhang et al, 2005). This KOR activation results in reduced dopamine and serotonin levels, contributing to the dysphoria-like behavioral responses that drive reinstatement of drug seeking and reward behaviors.…”

Section: Introductionmentioning

confidence: 99%

Locus Coeruleus Kappa-Opioid Receptors Modulate Reinstatement of Cocaine Place Preference Through a Noradrenergic Mechanism

Al‐Hasani

McCall

Foshage

et al. 2013

Neuropsychopharmacol

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Activation of kappa-opioid receptors (KORs) in monoamine circuits results in dysphoria-like behaviors and stress-induced reinstatement of drug seeking in both conditioned place preference (CPP) and self-administration models. Noradrenergic (NA) receptor systems have also been implicated in similar behaviors. Dynorphinergic projections terminate within the locus coeruleus (LC), a primary source of norepinephrine in the forebrain, suggesting a possible link between the NA and dynorphin/kappa opioid systems, yet the implications of these putative interactions have not been investigated. We isolated the necessity of KORs in the LC in kappa opioid agonist (U50,488)-induced reinstatement of cocaine CPP by blocking KORs in the LC with NorBNI (KOR antagonist). KOR-induced reinstatement was significantly attenuated in mice injected with NorBNI in the LC. To determine the sufficiency of KORs in the LC on U50,488-induced reinstatement of cocaine CPP, we virally re-expressed KORs in the LC of KOR knockout mice. We found that KORs expression in the LC alone was sufficient to partially rescue KOR-induced reinstatement. Next we assessed the role of NA signaling in KOR-induced reinstatement of cocaine CPP in the presence and absence of a a2-agonist (clonidine), b-adrenergic receptor antagonist (propranolol), and b 1 -and b 2 -antagonist (betaxolol and ICI-118,551 HCl). Both the blockade of postsynaptic b 1 -adrenergic receptors and the activation of presynaptic inhibitory adrenergic autoreceptors selectively potentiated the magnitude of KOR-induced reinstatement of cocaine CPP but not cocaine-primed CPP reinstatement. Finally, viral restoration of KORs in the LC together with b-adrenergic receptor blockade did not potentiate KOR-induced reinstatement to cocaine CPP, suggesting that adrenergic receptor interactions occur at KOR-expressing regions external to the LC. These results identify a previously unknown interaction between KORs and NA systems and suggest a NA regulation of KOR-dependent reinstatement of cocaine CPP.

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Effects of acute and repeated administration of salvinorin A on dopamine function in the rat dorsal striatum

Cited by 63 publications

References 31 publications

Neuropharmacology of the Naturally Occurring κ-Opioid Hallucinogen Salvinorin A

Neuropharmacology of the Naturally Occurring κ-Opioid Hallucinogen Salvinorin A

The role of κ-opioid receptor activation in mediating antinociception and addiction

Locus Coeruleus Kappa-Opioid Receptors Modulate Reinstatement of Cocaine Place Preference Through a Noradrenergic Mechanism

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