Axonal type 3 deiodinase in hypophysiotropic neurosecretory neurons responds to LPS treatment system-specifically

Program: Abstracts - Orals, Featured Poster Presentations, and Posters
Session: MON 414-436-HPT Axis Biology & Action
Monday, June 17, 2013: 1:45 PM-3:45 PM
Expo Halls ABC (Moscone Center)

Poster Board MON-426
Petra Mohacsik1, Rafael Arrojo e Drigo2, Liping Dong2, Antonio C Bianco3, Csaba Fekete1 and Balazs Gereben*1
1Institute of Experimental Med, Budapest, Hungary, 2Miller School of Medicine, University of Miami, Miami, FL, 3University of Miami Miller School of Medicine, Miami, FL
Thyroid hormones (TH) are key regulators of hypothalamic neurosecretory neurons influencing metabolism, growth, stress and reproduction. We have recently described a novel pathway of TH signaling in parvocellular neurosecretory neurons that involves  MCT8-mediated uptake of T3 into axon terminals from the median eminence (ME) followed by regulation of  intracellular T3 levels via type 3 deiodinase (D3). We also demonstrated that D3 distribution in  axon varicosities in the ME was highly cell-type dependent. In the present study, we assessed how D3-mediated T3 regulation in specific parvocellular neurons of rats responds to bacterial lipopolysaccharide (LPS), a factor known to induce hypothalamic T3 generation. In the ME,  D3 activity was not significantly changed but showed a tendency to increase, triggered by increased local T3 generation by hypothalamic tanycytes, that was in striking contrast to the 10-fold drop in cortical D3 activity to compensate for falling cortical T3 levels. Analysis of D3 distribution in hypohpysiotrop axons revealed, a significant decrease in the number of D3 positive CRH- (45%) and GHRH-immonoreactive (IR) (10%) varicosities in in the external zone of the median eminence, while the presence of D3 in GnRH- and TRH-IR varicosities did not change. Our data suggest that hypophysiotropic neurons can system-specifically influence their intracellular T3 levels by regulating their axonal D3 content to allow cell-type specific response to LPS challenge.

Nothing to Disclose: PM, RA, LD, ACB, CF, BG

*Please take note of The Endocrine Society's News Embargo Policy at

Sources of Research Support: This work was supported by the National Science Foundation of Hungary (OTKA K81226) and the European Community’s Seventh Framework Programme (FP7/2007-2013) under grant agreement no. 259772.