Submitted on August 19, 2002
Accepted on February 7, 2003
Norepinephrine release in brown adipose tissue remains robust in cold-exposed senescent Fischer 344 rats
Annette M Gabaldon1, David A Gavel2, Jock S Hamilton2, Roger B McDonald3, and Barbara A Horwitz2*
1 Department of Zoology, Oregon State University, Corvallis, CA, USA; Section of Neurobiology, Physiology, and Behavior, Division of Biological Scienes, University of California, Davis, CA, USA
2 Section of Neurobiology, Physiology, and Behavior, Division of Biological Scienes, University of California, Davis, CA, USA
3 Department of Nutrition, University of California, Davis, CA, USA
* To whom correspondence should be addressed. E-mail: bahorwitz{at}ucdavis.edu.
Near the end of life, old F344 rats undergo a transition, marked by spontaneous and rapidly declining function. Food intake and body weight decrease; and these rats, which we call senescent, develop severe hypothermia in the cold due in part to blunted brown fat (BAT) thermogenesis. We tested the hypothesis that this attenuation may involve diminished sympathetic signaling by measuring cold-induced BAT norepinephrine release in freely moving rats using linear microdialysis probes surgically implanted into interscapular BAT 24 and 48 h previously. In response to 2 h at 15°C, senescent rats increased BAT norepinephrine release 6- to 10-fold but did not maintain homeothermy. This increase was comparable to that of old presenescent (weight-stable) rats that did maintain homeothermy during even greater cold exposure (2 h at 15°C followed by 1.5 h at 8°C). Tail temperatures, an index of vasoconstrictor responsiveness to cold, exhibited similar cooling curves in presenescent and senescent rats. Thus, cold-induced sympathetic signaling to BAT and tail vasoconstrictor responsiveness remain robust in senescent rats and cannot explain their cold-induced hypothermia.
