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Submitted on December 2, 2005
Accepted on April 10, 2006
Division of Endocrinology, Department of Medicine, Brown Medical School/Rhode Island Hospital, Providence, RI 02903, Department of Molecular Biology, Cell Biology and Biochemistry, Brown University, RI 02903
* To whom correspondence should be addressed. E-mail: Eduardo_Nillni{at}Brown.edu.
We have previously shown that leptin regulates proThyrotropin Releasing Hormone (proTRH) in the paraventricular nucleus (PVN) of the hypothalamus through two pathways. The first one acts directly on proTRH neurons, and the second one (indirect) acts through the melanocorting system (arcuate nucleus, ARC). However, it is unknown whether the direct or the indirect pathways of leptin action on proTRH neurons occurs on separated or on the same subsets of neurons within the PVN region. We used immunostaining for the Phosphorylated Signal Transducer and Activator of Transcription 3 (P-STAT3) to localize direct leptin signaling, and the Phosphorylated cAMP Response Element Binding protein (P-CREB) to localize indirect signaling on proTRH neurons in animals ICV (intra cerebro ventricular) injected with leptin. With this approach we were able to identify two subsets of neuronal populations responsive to leptin, which are distributed in different regions within the PVN. ProTRH neurons directly responsive to leptin were located mainly in the medial and posterior part of the PVN, and they were not primarily related to the hypothalamic pituitary thyroid (HPT) axis. Whereas, proTRH neurons indirectly responsive (through 
-MSH) to leptin were located mainly in the anterior, medial and periventricular part of the PVN, and related to the HPT axis. In addition, -MSH showed to affect the processing of proTRH and up-regulated the prohormone convertase 1/3. We showed here evidence supporting the hypothesis that in the PVN there are subpopulations of proTRH neurons responding to leptin, which is dependent upon the way leptin reaches its primary target(s) in the hypothalamus. These findings are critical to a better understanding of leptin-mediated actions in energy expenditure.
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