@article {4605,
	title = {Leptin targets in the mouse brain.},
	journal = {The Journal of Comparative Neurology},
	volume = {514},
	year = {2009},
	month = {2009 Jun 10},
	pages = {518-32},
	abstract = {<p>The central actions of leptin are essential for homeostatic control of adipose tissue mass, glucose metabolism, and many autonomic and neuroendocrine systems. In the brain, leptin acts on numerous different cell types via the long-form leptin receptor (LepRb) to elicit its effects. The precise identification of leptin{\textquoteright}s cellular targets is fundamental to understanding the mechanism of its pleiotropic central actions. We have systematically characterized LepRb distribution in the mouse brain using in situ hybridization in wildtype mice as well as by EYFP immunoreactivity in a novel LepRb-IRES-Cre EYFP reporter mouse line showing high levels of LepRb mRNA/EYFP coexpression. We found substantial LepRb mRNA and EYFP expression in hypothalamic and extrahypothalamic sites described before, including the dorsomedial nucleus of the hypothalamus, ventral premammillary nucleus, ventral tegmental area, parabrachial nucleus, and the dorsal vagal complex. Expression in insular cortex, lateral septal nucleus, medial preoptic area, rostral linear nucleus, and in the Edinger-Westphal nucleus was also observed and had been previously unreported. The LepRb-IRES-Cre reporter line was used to chemically characterize a population of leptin receptor-expressing neurons in the midbrain. Tyrosine hydroxylase and Cre reporter were found to be coexpressed in the ventral tegmental area and in other midbrain dopaminergic neurons. Lastly, the LepRb-IRES-Cre reporter line was used to map the extent of peripheral leptin sensing by central nervous system (CNS) LepRb neurons. Thus, we provide data supporting the use of the LepRb-IRES-Cre line for the assessment of the anatomic and functional characteristics of neurons expressing leptin receptor.</p>
},
	keywords = {Animals, Brain, Cell Count, Gene Expression, Immunohistochemistry, In Situ Hybridization, Lac Operon, Leptin, Male, Messenger, Mice, Photomicrography, Receptors, RNA, STAT3 Transcription Factor, Transgenic, Tyrosine 3-Monooxygenase},
	issn = {1096-9861},
	doi = {10.1002/cne.22025},
	author = {Scott, Michael M and Lachey, Jennifer L and Sternson, Scott M and Lee, Charlotte E and Elias, Carol F and Friedman, Jeffrey M and Elmquist, Joel K}
}
@article {2187,
	title = {Topographic mapping of VMH {\textendash}> arcuate nucleus microcircuits and their reorganization by fasting.},
	journal = {Nature Neuroscience},
	volume = {8},
	year = {2005},
	month = {2005 Oct},
	pages = {1356-63},
	abstract = {<p>In the hypothalamic arcuate nucleus (ARC), pro-opiomelanocortin (POMC) neurons inhibit feeding and neuropeptide-Y (NPY) neurons stimulate feeding. We tested whether neurons in the ventromedial hypothalamic nucleus (VMH), a known satiety center, activate anorexigenic neuronal pathways in the ARC by projecting either excitatory synaptic inputs to POMC neurons and/or inhibitory inputs to NPY neurons. Using laser scanning photostimulation in brain slices from transgenic mice, we found that POMC and NPY neurons, which are interspersed in the ARC, are nevertheless regulated by anatomically distinct synaptic inputs. POMC neurons received strong excitatory input from the medial VMH (mVMH), whereas NPY neurons did not and, instead, received weak inhibitory input only from within the ARC. The strength of the excitatory input from the mVMH to POMC neurons was diminished by fasting. These data identify a new molecularly defined circuit that is dynamically regulated by nutritional state in a manner consistent with the known role of the VMH as a satiety center.</p>
},
	keywords = {Action Potentials, Animals, Arcuate Nucleus, Brain Mapping, Fasting, Glutamic Acid, Immunohistochemistry, Lasers, Leptin, Male, Mice, Nerve Net, Neural Networks (Computer), Neuronal Plasticity, Neurons, Neuropeptide Y, Newborn, Patch-Clamp Techniques, Photic Stimulation, Pro-Opiomelanocortin, Synapses, Transgenic},
	issn = {1097-6256},
	doi = {10.1038/nn1550},
	author = {Sternson, Scott M and Shepherd, Gordon M G and Friedman, Jeffrey M}
}
