Leptin receptor signaling in midbrain dopamine neurons regulates feeding.

By Jonathan D. Hommel, R. Trinko, Robert M. Sears, D. Georgescu, Zong-Wu Liu, Xiao-Bing Gao, J. Thurmon, M. Marinelli, R. DiLeone. Neuron, 2006

921 citations recorded by the source corpus.

Subfields: Cognitive Neuroscience, Endocrine and Autonomic Systems, Nutrition and Dietetics

View Paper: https://www.semanticscholar.org/paper/d76711c3f26fb52db06d37d92b4d65a0b5e3c036

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Citations in the corpus

Pathophysiology of Migraine: A Disorder of Sensory Processing. (2017, background): “The VTA is implicated in modulating food craving behaviors (600), as well as the drive to access highly palatable foods (3, 4), and increased leptin signaling in the VTA decreases food intake and firing rates of DA neurons (287, 414).”
Projection-specific modulation of dopamine neuron synapses by aversive and rewarding stimuli (2011, neutral): “…2001; Gutlerner et al., 2002; Saal et al., 2003; Borgland et al., 2004; Faleiro et al., 2004; Bellone and Lü scher, 2006; Margolis et al., 2006; Hommel et al., 2006; Argilli et al., 2008; Stuber et al., 2008; Zweifel et al., 2008) even though this criterion does not unequivocally identify DA…”
The mammalian circadian timing system: organization and coordination of central and peripheral clocks. (2010, background): “In particular, leptin reduces the firing rates of dopaminergic neurons (175), indicating that leptin exerts a direct influence on dopamine neurons via leptin receptors in the VTA (176).”
Mechanisms of leptin action and leptin resistance. (2008, background): “Although ARC LRb neurons do not project to the VTA and there is little evidence for the modulation of the mesolimbic circuitry by NPY or melanocortin action, a number of research groups have demonstrated the presence of LRb-expressing VTA DA neurons and proven the ability of leptin to alter the phys”
The tempted brain eats: pleasure and desire circuits in obesity and eating disorders. (2010, background): “It is also noteworthy that endocannabinoids also facilitate mesolimbic dopamine via the ventral tegmental area and other sites, which might facilitate the incentive salience “wanting” of palatable foods independently of hedonic “liking” (Cota et al., 2006; Kirkham, 2005).”
Addiction-like reward dysfunction and compulsive eating in obese rats: Role for dopamine D2 receptors (2010, background): “Recent reports indicate that circulating leptin, a key regulator of energy balance, can penetrate into brain tissues and inhibit the activity of reward circuit”
‘Liking’ and ‘wanting’ food rewards: Brain substrates and roles in eating disorders (2009, neutral): “[103,186–190].”
Food reward in the absence of taste receptor signaling. (2008, positive): “We thus reason that the putative role of dopamine transmission in overeating and obesity might not be restricted to oral hedonics; rather, dopamine signaling could influence behavior also by coding for the food’s nutritive value (Figlewicz, 2003; Fulton et al., 2006; Hommel et al., 2006; Palmiter,”
An opportunity cost model of subjective effort and task performance (2013, positive): “Consider that glucose is known to act on the brain’s reward circuitry, both through receptors on dopamine neurons (Hommel et al. 2006) and indirectly (i.e., with delivery of glucose into the mouth; McClure et al. 2003; O’Doherty et al. 2003).”
The Hormonal Control of Food Intake (2007, positive): “Two recent studies now clearly indicate that by acting upon these dopaminergic neurons, leptin influences food consumption in a hitherto unrecognized manner (Fulton et al., 2006; Hommel et al., 2006).”
Physiology of leptin: energy homeostasis, neuroendocrine function and metabolism. (2015, background): “Moreover, leptin modulates the mesolimbic dopamine system indirectly through the lateral hypothalamus [25, 40].”