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Peng Xu, John J Gildea, Chi Zhang, Prasad Konkalmatt, Santiago Cuevas, Dora Bigler Wang, Hanh T Tran, Pedro A Jose, and Robin A Felder

Gastrin, secreted by stomach G cells in response to ingested sodium, stimulates the renal cholecystokinin B receptor (CCKBR) to increase renal sodium excretion. It is not known how dietary sodium, independent of food, can increase gastrin secretion in human G cells. However, fenofibrate (FFB), a peroxisome proliferator-activated receptor-α (PPAR-α) agonist, increases gastrin secretion in rodents and several human gastrin-secreting cells, via a gastrin transcriptional promoter. We tested the following hypotheses: (1.) the sodium sensor in G cells plays a critical role in the sodium-mediated increase in gastrin expression/secretion, and (2.) dopamine, via the D1R and PPAR-α, is involved. Intact human stomach antrum and G cells were compared with human gastrin-secreting gastric and ovarian adenocarcinoma cells. When extra- or intracellular sodium was increased in human antrum, human G cells, and adenocarcinoma cells, gastrin mRNA and protein expression/secretion were increased. In human G cells, the PPAR-α agonist FFB increased gastrin protein expression that was blocked by GW6471, a PPAR-α antagonist, and LE300, a D1-like receptor antagonist. LE300 prevented the ability of FFB to increase gastrin protein expression in human G cells via the D1R, because the D5R, the other D1-like receptor, is not expressed in human G cells. Human G cells also express tyrosine hydroxylase and DOPA decarboxylase, enzymes needed to synthesize dopamine. G cells in the stomach may be the sodium sensor that stimulates gastrin secretion, which enables the kidney to eliminate acutely an oral sodium load. Dopamine, via the D1R, by interacting with PPAR-α, is involved in this process.

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David Aguinaga, Mireia Casanovas, Rafael Rivas-Santisteban, Irene Reyes-Resina, Gemma Navarro, and Rafael Franco

repeated exposure to cocaine. This conclusion arises from data in ERK1 KO mice, which display a facilitation of acquisition of cocaine CPP and of locomotor sensitization ( Ferguson et al. 2006 ). Also interesting is the finding that dopamine D 1 receptor

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Bice Chini and Marco Parenti

function – the hydrophobic matching hypothesis revisited . Biochimica et Biophysica Acta 1666 205 – 226 . Jin H Zastawny R George SR O'Dowd BF 1997 Elimination of palmitoylation sites in the human dopamine D1 receptor does not affect

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A R Rodrigues, D Sousa, H Almeida, and A M Gouveia

-terminal motifs seem to be involved in the intracellular trafficking of GPCRs from ER to cell surface, such as the triple phenylalanine motif F(X) 3 F(X) 3 F identified in the dopamine D1 receptor ( Bermak et al . 2001 ) and the di-leucine motif E(X) 3 LL of the

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Gunnar Kleinau, Anne Müller, and Heike Biebermann

290 3875 – 3892 . ( doi:10.1074/jbc.M114.622498 ) Juhasz JR Hasbi A Rashid AJ So CH George SR O’Dowd BF 2008 Mu-opioid receptor heterooligomer formation with the dopamine D1 receptor as directly visualized in living cells

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Joram D Mul

Parker KE Childs TE Will MJ Booth FW 2012 Dopamine D1 receptor modulation in nucleus accumbens lowers voluntary wheel running in rats bred to run high distances . Physiology and Behavior 105 661 – 668 . ( https://doi.org/10.1016/j