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Dopamine signaling in reward-related behaviors.

Baik JH - Front Neural Circuits (2013)

Bottom Line: Dopamine (DA) regulates emotional and motivational behavior through the mesolimbic dopaminergic pathway.Changes in DA mesolimbic neurotransmission have been found to modify behavioral responses to various environmental stimuli associated with reward behaviors.Psychostimulants, drugs of abuse, and natural reward such as food can cause substantial synaptic modifications to the mesolimbic DA system.

View Article: PubMed Central - PubMed

Affiliation: Molecular Neurobiology Laboratory, Department of Life Sciences, Korea University Seoul, South Korea.

ABSTRACT
Dopamine (DA) regulates emotional and motivational behavior through the mesolimbic dopaminergic pathway. Changes in DA mesolimbic neurotransmission have been found to modify behavioral responses to various environmental stimuli associated with reward behaviors. Psychostimulants, drugs of abuse, and natural reward such as food can cause substantial synaptic modifications to the mesolimbic DA system. Recent studies using optogenetics and DREADDs, together with neuron-specific or circuit-specific genetic manipulations have improved our understanding of DA signaling in the reward circuit, and provided a means to identify the neural substrates of complex behaviors such as drug addiction and eating disorders. This review focuses on the role of the DA system in drug addiction and food motivation, with an overview of the role of D1 and D2 receptors in the control of reward-associated behaviors.

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Related in: MedlinePlus

D2 receptor-mediated ERK activation signaling pathway. D2 receptor-mediated ERK activation is dependent on Gαi protein coupling. It also appears that D2 receptor-mediated ERK activation requires the transactivation of receptor tyrosine kinase, which consequently activates downstream signaling involving matrix metalloproteinases (MMPs) with ectodomain shedding of EGFR ligand, for example, to finally activate ERK (Choi et al., 1999; Kim et al., 2004; Wang et al., 2005; ). The involvement of arrestin has also been suggested to contribute to D2 receptor-mediated ERK activation (Beom et al., 2004; Kim et al., 2004), which can activate MAPK signaling by mobilizing clathrin-mediated endocytosis in a β-arrestin/dynamin-dependent manner (Kim et al., 2004).
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Figure 2: D2 receptor-mediated ERK activation signaling pathway. D2 receptor-mediated ERK activation is dependent on Gαi protein coupling. It also appears that D2 receptor-mediated ERK activation requires the transactivation of receptor tyrosine kinase, which consequently activates downstream signaling involving matrix metalloproteinases (MMPs) with ectodomain shedding of EGFR ligand, for example, to finally activate ERK (Choi et al., 1999; Kim et al., 2004; Wang et al., 2005; ). The involvement of arrestin has also been suggested to contribute to D2 receptor-mediated ERK activation (Beom et al., 2004; Kim et al., 2004), which can activate MAPK signaling by mobilizing clathrin-mediated endocytosis in a β-arrestin/dynamin-dependent manner (Kim et al., 2004).

Mentions: D2 receptor-mediated ERK activation has been reported in heterologous cell culture systems (Luo et al., 1998; Welsh et al., 1998; Choi et al., 1999). D2 receptor-mediated ERK activation was found to be dependent on Gαi protein coupling, and it appears thatit requires the transactivation of receptor tyrosine kinase, which activates downstream signaling to finally activate ERK (Choi et al., 1999; Kim et al., 2004; Wang et al., 2005; Yoon et al., 2011; Yoon and Baik, 2013). Arrestin has been also suggested to contribute to D2 receptor-mediated ERK activation (Beom et al., 2004; Kim et al., 2004), which can activate MAPK signaling by mobilizing clathrin-mediated endocytosis in a β-arrestin/dynamin-dependent manner (Kim et al., 2004). A further possibility of D2 receptorscoupling to Gq proteins cannot be ruled out; in this case, Gq protein-mediated PKC activation could also induce ERK activation (Choi et al., 1999; Figure 2).


Dopamine signaling in reward-related behaviors.

Baik JH - Front Neural Circuits (2013)

D2 receptor-mediated ERK activation signaling pathway. D2 receptor-mediated ERK activation is dependent on Gαi protein coupling. It also appears that D2 receptor-mediated ERK activation requires the transactivation of receptor tyrosine kinase, which consequently activates downstream signaling involving matrix metalloproteinases (MMPs) with ectodomain shedding of EGFR ligand, for example, to finally activate ERK (Choi et al., 1999; Kim et al., 2004; Wang et al., 2005; ). The involvement of arrestin has also been suggested to contribute to D2 receptor-mediated ERK activation (Beom et al., 2004; Kim et al., 2004), which can activate MAPK signaling by mobilizing clathrin-mediated endocytosis in a β-arrestin/dynamin-dependent manner (Kim et al., 2004).
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC3795306&req=5

Figure 2: D2 receptor-mediated ERK activation signaling pathway. D2 receptor-mediated ERK activation is dependent on Gαi protein coupling. It also appears that D2 receptor-mediated ERK activation requires the transactivation of receptor tyrosine kinase, which consequently activates downstream signaling involving matrix metalloproteinases (MMPs) with ectodomain shedding of EGFR ligand, for example, to finally activate ERK (Choi et al., 1999; Kim et al., 2004; Wang et al., 2005; ). The involvement of arrestin has also been suggested to contribute to D2 receptor-mediated ERK activation (Beom et al., 2004; Kim et al., 2004), which can activate MAPK signaling by mobilizing clathrin-mediated endocytosis in a β-arrestin/dynamin-dependent manner (Kim et al., 2004).
Mentions: D2 receptor-mediated ERK activation has been reported in heterologous cell culture systems (Luo et al., 1998; Welsh et al., 1998; Choi et al., 1999). D2 receptor-mediated ERK activation was found to be dependent on Gαi protein coupling, and it appears thatit requires the transactivation of receptor tyrosine kinase, which activates downstream signaling to finally activate ERK (Choi et al., 1999; Kim et al., 2004; Wang et al., 2005; Yoon et al., 2011; Yoon and Baik, 2013). Arrestin has been also suggested to contribute to D2 receptor-mediated ERK activation (Beom et al., 2004; Kim et al., 2004), which can activate MAPK signaling by mobilizing clathrin-mediated endocytosis in a β-arrestin/dynamin-dependent manner (Kim et al., 2004). A further possibility of D2 receptorscoupling to Gq proteins cannot be ruled out; in this case, Gq protein-mediated PKC activation could also induce ERK activation (Choi et al., 1999; Figure 2).

Bottom Line: Dopamine (DA) regulates emotional and motivational behavior through the mesolimbic dopaminergic pathway.Changes in DA mesolimbic neurotransmission have been found to modify behavioral responses to various environmental stimuli associated with reward behaviors.Psychostimulants, drugs of abuse, and natural reward such as food can cause substantial synaptic modifications to the mesolimbic DA system.

View Article: PubMed Central - PubMed

Affiliation: Molecular Neurobiology Laboratory, Department of Life Sciences, Korea University Seoul, South Korea.

ABSTRACT
Dopamine (DA) regulates emotional and motivational behavior through the mesolimbic dopaminergic pathway. Changes in DA mesolimbic neurotransmission have been found to modify behavioral responses to various environmental stimuli associated with reward behaviors. Psychostimulants, drugs of abuse, and natural reward such as food can cause substantial synaptic modifications to the mesolimbic DA system. Recent studies using optogenetics and DREADDs, together with neuron-specific or circuit-specific genetic manipulations have improved our understanding of DA signaling in the reward circuit, and provided a means to identify the neural substrates of complex behaviors such as drug addiction and eating disorders. This review focuses on the role of the DA system in drug addiction and food motivation, with an overview of the role of D1 and D2 receptors in the control of reward-associated behaviors.

Show MeSH
Related in: MedlinePlus