Serotonin 2C receptor activates a distinct population of arcuate pro-opiomelanocortin neurons via TRPC channels

Jong Woo Sohn; Yong Xu; Juli E. Jones; Kevin Wickman; Kevin W. Williams; Joel K. Elmquist

doi:10.1016/j.neuron.2011.06.012

Serotonin 2C receptor activates a distinct population of arcuate pro-opiomelanocortin neurons via TRPC channels

Jong Woo Sohn, Yong Xu, Juli E. Jones, Kevin Wickman, Kevin W. Williams, Joel K. Elmquist

Pharmacology

Research output: Contribution to journal › Article › peer-review

167 Scopus citations

Abstract

Serotonin 2C receptors (5-HT_2CRs) expressed by pro-opiomelanocortin (POMC) neurons of hypothalamic arcuate nucleus regulate food intake, energy homeostasis and glucose metabolism. However, the cellular mechanisms underlying the effects of 5-HT to regulate POMC neuronal activity via 5-HT_2CRs have not yet been identified. In the present study, we found the putative transient receptor potential C (TRPC) channels mediate the activation of a subpopulation of POMC neurons by mCPP (a 5-HT_2CR agonist). Interestingly, mCPP-activated POMC neurons were found to be a distinct population from those activated by leptin. Together, our data suggest that 5-HT_2CR and leptin receptors are expressed by distinct subpopulations of arcuate POMC neurons and that both 5-HT and leptin exert their actions in POMC neurons via TRPC channels.

Original language	English (US)
Pages (from-to)	488-497
Number of pages	10
Journal	Neuron
Volume	71
Issue number	3
DOIs	https://doi.org/10.1016/j.neuron.2011.06.012
State	Published - Aug 11 2011

Bibliographical note

Funding Information:
We thank Dr. Jefferey Friedman (Rockefeller University) for kindly providing us with the LepR-cre mice. This work was supported by grants to J.-W.S. (American Diabetes Association), Y.X. (R00DK085330, P30DK079638-03, American Diabetes Association, and the Naman Family Fund for Basic Research and the Curtis Hankamer Basic Research Fund), K.W. (R01MH061933, P50DA011806), K.W.W. (K01DK087780), and J.K.E. (R01DK53301, R01DK088423, and RL1DK081185). This work was also supported by PL1 DK081182 and UL1RR024923.

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title = "Serotonin 2C receptor activates a distinct population of arcuate pro-opiomelanocortin neurons via TRPC channels",

abstract = "Serotonin 2C receptors (5-HT2CRs) expressed by pro-opiomelanocortin (POMC) neurons of hypothalamic arcuate nucleus regulate food intake, energy homeostasis and glucose metabolism. However, the cellular mechanisms underlying the effects of 5-HT to regulate POMC neuronal activity via 5-HT2CRs have not yet been identified. In the present study, we found the putative transient receptor potential C (TRPC) channels mediate the activation of a subpopulation of POMC neurons by mCPP (a 5-HT2CR agonist). Interestingly, mCPP-activated POMC neurons were found to be a distinct population from those activated by leptin. Together, our data suggest that 5-HT2CR and leptin receptors are expressed by distinct subpopulations of arcuate POMC neurons and that both 5-HT and leptin exert their actions in POMC neurons via TRPC channels.",

author = "Sohn, {Jong Woo} and Yong Xu and Jones, {Juli E.} and Kevin Wickman and Williams, {Kevin W.} and Elmquist, {Joel K.}",

note = "Funding Information: We thank Dr. Jefferey Friedman (Rockefeller University) for kindly providing us with the LepR-cre mice. This work was supported by grants to J.-W.S. (American Diabetes Association), Y.X. (R00DK085330, P30DK079638-03, American Diabetes Association, and the Naman Family Fund for Basic Research and the Curtis Hankamer Basic Research Fund), K.W. (R01MH061933, P50DA011806), K.W.W. (K01DK087780), and J.K.E. (R01DK53301, R01DK088423, and RL1DK081185). This work was also supported by PL1 DK081182 and UL1RR024923. ",

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AU - Wickman, Kevin

AU - Williams, Kevin W.

AU - Elmquist, Joel K.

N1 - Funding Information: We thank Dr. Jefferey Friedman (Rockefeller University) for kindly providing us with the LepR-cre mice. This work was supported by grants to J.-W.S. (American Diabetes Association), Y.X. (R00DK085330, P30DK079638-03, American Diabetes Association, and the Naman Family Fund for Basic Research and the Curtis Hankamer Basic Research Fund), K.W. (R01MH061933, P50DA011806), K.W.W. (K01DK087780), and J.K.E. (R01DK53301, R01DK088423, and RL1DK081185). This work was also supported by PL1 DK081182 and UL1RR024923.

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N2 - Serotonin 2C receptors (5-HT2CRs) expressed by pro-opiomelanocortin (POMC) neurons of hypothalamic arcuate nucleus regulate food intake, energy homeostasis and glucose metabolism. However, the cellular mechanisms underlying the effects of 5-HT to regulate POMC neuronal activity via 5-HT2CRs have not yet been identified. In the present study, we found the putative transient receptor potential C (TRPC) channels mediate the activation of a subpopulation of POMC neurons by mCPP (a 5-HT2CR agonist). Interestingly, mCPP-activated POMC neurons were found to be a distinct population from those activated by leptin. Together, our data suggest that 5-HT2CR and leptin receptors are expressed by distinct subpopulations of arcuate POMC neurons and that both 5-HT and leptin exert their actions in POMC neurons via TRPC channels.

AB - Serotonin 2C receptors (5-HT2CRs) expressed by pro-opiomelanocortin (POMC) neurons of hypothalamic arcuate nucleus regulate food intake, energy homeostasis and glucose metabolism. However, the cellular mechanisms underlying the effects of 5-HT to regulate POMC neuronal activity via 5-HT2CRs have not yet been identified. In the present study, we found the putative transient receptor potential C (TRPC) channels mediate the activation of a subpopulation of POMC neurons by mCPP (a 5-HT2CR agonist). Interestingly, mCPP-activated POMC neurons were found to be a distinct population from those activated by leptin. Together, our data suggest that 5-HT2CR and leptin receptors are expressed by distinct subpopulations of arcuate POMC neurons and that both 5-HT and leptin exert their actions in POMC neurons via TRPC channels.

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Serotonin 2C receptor activates a distinct population of arcuate pro-opiomelanocortin neurons via TRPC channels

Abstract

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