Microinjection of CART (cocaine- and amphetamine-regulated transcript) peptide into the nucleus accumbens inhibits the cocaine-induced upregulation of dopamine receptors and locomotor sensitization

Peng, Qinghua; Sun, Xi; Liu, Ziyong; Yang, Jianghua; Oh, Ki‐Wan; Hu, Zhenzhen

doi:10.1016/j.neuint.2014.06.005

Cited by 19 publications

(14 citation statements)

References 38 publications

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“…; Peng et al . ). However, CaMKIIα not only regulates CREB expression (Wu and McMurray ) but also interacts with D3Rs, thereby decreasing the efficiency of the receptor (Liu et al .…”

Section: Discussionmentioning

confidence: 97%

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Cocaine‐ and amphetamine‐regulated transcript peptide in the nucleus accumbens shell inhibits cocaine‐induced locomotor sensitization to transient over‐expression of α‐Ca²⁺/calmodulin‐dependent protein kinase II

Xiong

Meng

Sun

et al. 2018

Journal of Neurochemistry

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Cocaine- and amphetamine-regulated transcript (CART) peptide is a widely distributed neurotransmitter that attenuates cocaine-induced locomotor activity when injected into the nucleus accumbens (NAc). Our previous work first confirmed that the inhibitory mechanism of the CART peptide on cocaine-induced locomotor activity is related to a reduction in cocaine-enhanced phosphorylated Ca /calmodulin-dependent protein kinaseIIα (pCaMKIIα) and the enhancement of cocaine-induced D3R function. This study investigated whether CART peptide inhibited cocaine-induced locomotor activity via inhibition of interactions between pCaMKIIα and the D3 dopamine receptor (D3R). We demonstrated that lentivirus-mediated gene transfer transiently increased pCaMKIIα expression, which peaked at 10 days after microinjection into the rat NAc shell, and induced a significant increase in Ca influx along with greater behavioral sensitivity in the open field test after intraperitoneal injections of cocaine (15 mg/kg). However, western blot analysis and coimmunoprecipitation demonstrated that CART peptide treatment in lentivirus-transfected CaMKIIα-over-expressing NAc rat tissues or cells prior to cocaine administration inhibited the cocaine-induced Ca influx and attenuated the cocaine-increased pCaMKIIα expression in lentivirus-transfected CaMKIIα-over-expressing cells. CART peptide decreased the cocaine-enhanced phosphorylated cAMP response element binding protein (pCREB) expression via inhibition of the pCaMKIIα-D3R interaction, which may account for the prolonged locomotor sensitization induced by repeated cocaine treatment in lentivirus-transfected CaMKIIα-over-expressing cells. These results provide strong evidence for the inhibitory modulation of CART peptide in cocaine-induced locomotor sensitization. Cover Image for this issue: doi: 10.1111/jnc.14187.

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“…; Peng et al . ). However, CaMKIIα not only regulates CREB expression (Wu and McMurray ) but also interacts with D3Rs, thereby decreasing the efficiency of the receptor (Liu et al .…”

Section: Discussionmentioning

confidence: 97%

“…; Peng et al . ), which suggests that the CART peptide may be a potential target for the treatment of cocaine addiction. However, the specific mechanisms of the intra‐accumbal injected CART peptide attenuation of cocaine‐induced behavioral sensitivity are not clear.…”

mentioning

confidence: 99%

Cocaine‐ and amphetamine‐regulated transcript peptide in the nucleus accumbens shell inhibits cocaine‐induced locomotor sensitization to transient over‐expression of α‐Ca²⁺/calmodulin‐dependent protein kinase II

Xiong

Meng

Sun

et al. 2018

Journal of Neurochemistry

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“…Central injection of CART showed reduced locomotor sensitivity to cocaine through the inhibition of the upregulation of the dopamine receptor [31] . Nonetheless, orexigenic peptides or agouti-related peptide injection to the brain reduces TH in dopaminergic neurons [32] , while peptide YY (PYY) reduces the dopamine release in the hypothalamus [33] .…”

Section: Dopamine and Serotonin In Obesitymentioning

confidence: 96%

Khat (<b><i>Catha edulis</i></b>) and Obesity: A Scoping Review of Animal and Human Studies

et al. 2016

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Background: Khat (Catha edulis) is a plant that is deeply rooted in the cultural life of East African and Southwestern Arabian populations. Prevalent traditional beliefs about khat are that the plant has an effect on appetite and body weight. Summary: This review assesses the accumulated evidences on the mutual influence of monoamines, hormones and neuropeptides that are linked to obesity. A few anti-obesity drugs that exert their mechanisms of action through monoamines are briefly discussed to support the notion of monoamines being a critical target of drug discovery for new anti-obesity drugs. Subsequently, the review provides a comprehensive overview of central dopamine and serotonin changes that are associated with the use of khat or its alkaloids. Then, all the studies on khat that describe physical, biochemical and hormonal changes are summarised and discussed in depth. Conclusion: The reviewed studies provide relatively acceptable evidence that different khat extracts or cathinone produces changes in terms of weight, fat mass, appetite, lipid biochemistry and hormonal levels. These changes are more pronounced at higher doses and long durations of intervention. The most suggested mechanism of these changes is the central action that produces changes in the physiology of dopamine and serotonin. Nonetheless, there are a number of variations in the study design, including species, doses and durations of intervention, which makes it difficult to arrive at a final conclusion about khat regarding obesity, and further studies are necessary in the future to overcome these limitations.

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“…Similar to acute cocaine, MEK/ERK activation is necessary for the chronic cocaine-induced IEG expression in the CPu, NAc and Amy in a time-dependent manner 66,67 . In cocaine-sensitized animals, 7–21 days but not 1 day withdrawal resulted in increased Glu aminomethyl phosphonic acid receptor (AMPA-R) subunit surface insertion and NDMA-R subunit expression with paralleled pERK induction in the NAc 84–87 (also see 88 ). AMPA-R expression in the NAc after prolonged withdrawal from repeated cocaine injection is dependent on the activation of both GluN2B and pERK, which contributes to the development of behavioral sensitization 86 .…”

Section: Erk Signaling and Drug Addictionmentioning

confidence: 97%

Molecular Mechanism: ERK Signaling, Drug Addiction, and Behavioral Effects

Sun

Quizon

Zhu

2016

Progress in Molecular Biology and Translational Science

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Addiction to psychostimulants has been considered as a chronic psychiatric disorder, characterized by craving and compulsive drug seeking and use. Over the past two decades, accumulating evidence has demonstrated that repeated drug exposure causes long-lasting neurochemical and cellular changes that results in enduring neuroadaptation in brain circuitry and underlie compulsive drug consumption and relapse. Through intercellular signaling cascades, drugs of abuse induce remodeling in the rewarding circuitry that contributes to the neuroplasticity of learning and memory associated with addiction. Here, we review the role of the extracellular signal-regulated kinase (ERK), a member of the mitogen-activated protein kinase, and its related intracellular signaling pathways in drug-induced neuroadaptive changes that are associated with drug-mediated psychomotor activity, rewarding properties and relapse of drug seeking behaviors. We also discuss the neurobiological and behavioral effects of pharmacological and genetic interferences with ERK-associated molecular cascades in response to abused substances. Understanding the dynamic modulation of ERK signaling in response to drugs may provide novel molecular targets for therapeutic strategies to drug addiction.

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Microinjection of CART (cocaine- and amphetamine-regulated transcript) peptide into the nucleus accumbens inhibits the cocaine-induced upregulation of dopamine receptors and locomotor sensitization

Cited by 19 publications

References 38 publications

Cocaine‐ and amphetamine‐regulated transcript peptide in the nucleus accumbens shell inhibits cocaine‐induced locomotor sensitization to transient over‐expression of α‐Ca²⁺/calmodulin‐dependent protein kinase II

Cocaine‐ and amphetamine‐regulated transcript peptide in the nucleus accumbens shell inhibits cocaine‐induced locomotor sensitization to transient over‐expression of α‐Ca²⁺/calmodulin‐dependent protein kinase II

Khat (<b><i>Catha edulis</i></b>) and Obesity: A Scoping Review of Animal and Human Studies

Molecular Mechanism: ERK Signaling, Drug Addiction, and Behavioral Effects

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Microinjection of CART (cocaine- and amphetamine-regulated transcript) peptide into the nucleus accumbens inhibits the cocaine-induced upregulation of dopamine receptors and locomotor sensitization

Cited by 19 publications

References 38 publications

Cocaine‐ and amphetamine‐regulated transcript peptide in the nucleus accumbens shell inhibits cocaine‐induced locomotor sensitization to transient over‐expression of α‐Ca2+/calmodulin‐dependent protein kinase II

Cocaine‐ and amphetamine‐regulated transcript peptide in the nucleus accumbens shell inhibits cocaine‐induced locomotor sensitization to transient over‐expression of α‐Ca2+/calmodulin‐dependent protein kinase II

Khat (<b><i>Catha edulis</i></b>) and Obesity: A Scoping Review of Animal and Human Studies

Molecular Mechanism: ERK Signaling, Drug Addiction, and Behavioral Effects

Contact Info

Product

Resources

About

Cocaine‐ and amphetamine‐regulated transcript peptide in the nucleus accumbens shell inhibits cocaine‐induced locomotor sensitization to transient over‐expression of α‐Ca²⁺/calmodulin‐dependent protein kinase II

Cocaine‐ and amphetamine‐regulated transcript peptide in the nucleus accumbens shell inhibits cocaine‐induced locomotor sensitization to transient over‐expression of α‐Ca²⁺/calmodulin‐dependent protein kinase II