07.01.2013 Views

[Abstract Title]. - Society for Neuroscience

[Abstract Title]. - Society for Neuroscience

[Abstract Title]. - Society for Neuroscience

SHOW MORE
SHOW LESS

Create successful ePaper yourself

Turn your PDF publications into a flip-book with our unique Google optimized e-Paper software.

with the DMH as an important pathway <strong>for</strong> thermoregulatory adaptations via the preautonomic<br />

and neuroendocrine PVN. Furthermore, using pseudorabies virus (PRV) injections into brown<br />

adipose tissue (BAT) we found that indeed DMH/LepRb neurons are involved in the regulation<br />

of the sympathetic BAT input. In addition, PRV was detected within LepRb neurons of the<br />

retrochiasmatic hypothalamus/ARC and mPOA, areas that contain neurons that sense the<br />

circulation (e.g. leptin levels) and project to the DMH, suggesting that they may serve as sensory<br />

inputs into the DMH to regulate sympathetic PVN outputs to the BAT. There<strong>for</strong>e, DMH/LepRb<br />

neurons may mediate important aspects of leptin action on the ANS and neuroendocrine<br />

function. Grant support: AHA053298N and P/F DK020572-30 to HM; NARSAD Young<br />

Investigator Award to IAK.<br />

Disclosures: M. Faouzi, None; I. Kerman, None; G. Louis, None; R. Leshan, None; G.M.<br />

Leinninger, None; J.C. Jones, None; S.J. Watson, None; C.J. Rhodes, None; H. Munzberg ,<br />

None.<br />

Poster<br />

284. Regulation of Food Intake and Body Weight: Integration of Peripheral Signals:<br />

Systems<br />

Time: Sunday, November 16, 2008, 1:00 pm - 5:00 pm<br />

Program#/Poster#: 284.15/QQ10<br />

Topic: E.07.b. Integration of peripheral signals: Systems<br />

Support: NIH Grant NS52142<br />

NIH Grant HD47643<br />

NIH Grant DK56373<br />

<strong>Title</strong>: TNF activates astrocytes and catecholaminergic neurons in the solitary nucleus<br />

Authors: R. C. ROGERS, *G. E. HERMANN;<br />

Lab. Autonomic Neurosci, Pennington Biomed. Res. Ctr., Baton Rouge, LA<br />

<strong>Abstract</strong>: Tumor necrosis factor [TNF] produces a profound cachexia and anorexia associated<br />

with gastrointestinal stasis. Our work has suggested that the principal site of action of TNF to<br />

cause this change in gastric function is via vagal afferents within the nucleus of the solitary tract<br />

[NST]. Excitation of these afferents presumably causes gastric stasis by activating downstream<br />

NST neurons that, in turn, suppress gastric motility via action on neurons in the dorsal motor<br />

nucleus of the vagus that project to the stomach. Results from our parallel studies on gastric

Hooray! Your file is uploaded and ready to be published.

Saved successfully!

Ooh no, something went wrong!