cAMP-dependent protein kinase and reward-related learning: intra-accumbens Rp-cAMPS blocks amphetamine-produced place conditioning in rats

Beninger, Richard J.; Nakonechny, Patricia L.; Savina, Ioulia

doi:10.1007/s00213-003-1510-2

Cited by 36 publications

(39 citation statements)

References 37 publications

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“…been reported to attenuate amphetamine-induced place conditioning (41). These previous and present data suggest that the activation of PKA play an important role in EtOH-conditioned place preference.…”

Section: Discussionsupporting

confidence: 82%

Acamprosate Suppresses Ethanol-Induced Place Preference in Mice With Ethanol Physical Dependence

et al. 2013

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Section: Discussionsupporting

confidence: 82%

Acamprosate Suppresses Ethanol-Induced Place Preference in Mice With Ethanol Physical Dependence

et al. 2013

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“…Beninger et al (2003a) found that co-injections of amphetamine plus the PKA inhibitor Rp-cAMPS produced a dose-dependent blockade of the CPP effect. Rp-cAMPS or the PKA activator Sp-cAMPS alone failed to affect time spent on the drug-paired side.…”

Section: Pka and The Acquisition Of A Conditioned Place Preferencementioning

confidence: 98%

The role of signaling molecules in reward-related incentive learning

Beninger

Gerdjikov

2004

neurotox res

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Reward-related incentive learning involves the acquisition by neutral stimuli of an enhanced ability to elicit approach and other responses. Previous studies have shown that both dopamine (DA) and glutamate (Glu) play critical roles in this type of learning. Signaling molecules are intracellular messengers that participate in the influence of transmitter-receptor events on intracellular function including transcription in the nucleus. In recent years studies have begun to implicate signaling molecules in incentive learning. Thus, inhibition of cyclic adenosine monophosphate-dependent protein kinase (PKA) in the nucleus accumbens (NAc), that is activated by DA acting at D1-like receptors, blocks the acquisition of conditioned approach responses, lever pressing for food, conditioned place preference (CPP) based on NAc injections of amphetamine or cocaine, and conditioned activity based on NAc injections of amphetamine. Similar effects have been observed with PKA inhibition in the basolateral amygdala or medial prefrontal cortex. If animals were trained prior to testing with PKA inhibitors in NAc, no effect was seen suggesting that PKA is more important for acquisition than expression of incentive learning. Inhibition of calcium-dependent protein kinase or mitogen-activated protein kinases in NAc similarly has been shown to block the acquisition of incentive learning. Results support a model of DA-Glu synaptic interactions that form the basis of incentive learning.

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“…In addition to PKA (Wand et al, 2001;Beninger et al, 2003), protein kinase C (PKC) isoforms are implicated in a number of addictive behaviors (Cervo et al, 1997;Van der Zee and Douma, 1997;Pierce et al, 1998;Aujla and Beninger, 2003). However, the role of PKC in postsynaptic dopamine receptor signaling in the NAcb is poorly understood.…”

Section: Introductionmentioning

confidence: 99%

Atypical Protein Kinase C Is a Novel Mediator of Dopamine-Enhanced Firing in Nucleus Accumbens Neurons

Hopf¹,

Mailliard²,

Gonzalez³

et al. 2005

J. Neurosci.

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Current concepts suggest that nucleus accumbens (NAcb) dopamine mediates several motivated and addictive behaviors. Although the role of protein kinase A (PKA) and dopamine and cyclic adenosine 3Ј,5Ј monophosphate-regulated phosphoprotein 32 kDa in NAcb dopamine receptor throughput has been studied extensively, the contribution of protein kinase C (PKC) to NAcb firing is poorly understood. Here we show that dopamine-mediated enhancement of spike firing in NAcb shell medium spiny neurons was prevented by the PKC inhibitor bisindolylmaleimide but not by the phospholipase C inhibitor 1-[6-((17b-3-methoxyestra-1,3,5(10)-trien-17-yl) amino)hexyl]-1H-pyrrole-2,5-dione, suggesting a role for a diacylglycerol-independent atypical PKC (aPKC) isoform. In this regard, modulation of firing by dopamine was prevented by intracellular perfusion of a pseudosubstrate peptide inhibitor for aPKCs. We also provide evidence, using an in vitro kinase assay, that dopamine receptor activation increased aPKC activity in striatal membranes. Finally, direct activation of PKA with forskolin enhanced firing even during inhibition of aPKCs, suggesting that aPKCs acted upstream of PKA activation. Thus, aPKCs appear to mediate dopaminergic enhancement of spike firing in the NAcb shell, and may therefore play a critical role in NAcb-and dopamine-dependent goal-directed behaviors.

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cAMP-dependent protein kinase and reward-related learning: intra-accumbens Rp-cAMPS blocks amphetamine-produced place conditioning in rats

Abstract: Results supported the hypothesis that PKA activation in NAc is necessary for reward-related learning.

Cited by 36 publications

References 37 publications

Acamprosate Suppresses Ethanol-Induced Place Preference in Mice With Ethanol Physical Dependence

Acamprosate Suppresses Ethanol-Induced Place Preference in Mice With Ethanol Physical Dependence

The role of signaling molecules in reward-related incentive learning

Atypical Protein Kinase C Is a Novel Mediator of Dopamine-Enhanced Firing in Nucleus Accumbens Neurons

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