NPY-Y1 receptor antisense injected centrally in rats causes hyperthermia and feeding.
The central actions of neuropeptide Y antisense oligodeoxynucleotide (aNPY) and NPY-Y1 receptor antisense (aNPY-Y1) on body temperature (Tb), feeding and body weight of unrestrained rats were determined by the repeated intracerebroventricular (i.c.v.) injection of 0.5 microgram doses. aNPY-Y1 caused intense phasic rises in Tb, lowered body weight and caused transient feeding. aNPY increased food intake paradoxically, accompanied by a gain in body weight but did not affect Tb. Circadian activity was unaffected by either antisense oligodeoxynucleotide, and the mismatched NPY (mNPY) was without effect. These results show that NPY-Y1 receptors underlie the central thermolytic action of NPY, since aNPY-Y1 induces hyperthermic responses. Overall, the functional reduction in NPY activity by aNPY might cause a compensatory de novo synthesis of NPY in structures remote from the ventricles to augment feeding behavior.
Lopez-Valpuesta
F J
FJ
Department of Pharmacology, School of Medicine, East Carolina University, Greenville, NC 27858, USA.
Nyce
J W
JW
Myers
R D
RD
D000818:Animals; D001831:Body Temperature / Q000187:drug effects*; D005247:Feeding Behavior / Q000187:drug effects*; D007278:Injections, Spinal; D008297:Male; D016376:Oligonucleotides, Antisense / Q000494:pharmacology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D017476:Receptors, Neuropeptide Y / Q000187:drug effects*
D016376:Oligonucleotides, Antisense; D017476:Receptors, Neuropeptide Y