cgp-71683-a and Hypothermia

Exposure of chicks to a high ambient temperature (HT) has previously been shown to increase neuropeptide Y (NPY) mRNA expression in the brain. Furthermore, it was found that NPY has anti-stress functions in heat-exposed fasted chicks. The aim of the study was to reveal the role of central administration of NPY on thermotolerance ability and the induction of heat-shock protein (HSP) and NPY sub-receptors (NPYSRs) in fasted chicks with the contribution of plasma metabolite changes. Six- or seven-day-old chicks were centrally injected with 0 or 375 pmol of NPY and exposed to either HT (35 ± 1°C) or control thermoneutral temperature (CT: 30 ± 1°C) for 60 min while fasted. NPY reduced body temperature under both CT and HT NPY enhanced the brain mRNA expression of HSP-70 and -90, as well as of NPYSRs-Y5, -Y6, and -Y7, but not -Y1, -Y2, and -Y4, under CT and HT A coinjection of an NPYSR-Y5 antagonist (CGP71683) and NPY (375 pmol) attenuated the NPY-induced hypothermia. Furthermore, central NPY decreased plasma glucose and triacylglycerol under CT and HT and kept plasma corticosterone and epinephrine lower under HT NPY increased plasma taurine and anserine concentrations. In conclusion, brain NPYSR-Y5 partially afforded protective thermotolerance in heat-exposed fasted chicks. The NPY-mediated reduction in plasma glucose and stress hormone levels and the increase in free amino acids in plasma further suggest that NPY might potentially play a role in minimizing heat stress in fasted chicks.

Topics: Adaptation, Physiological; Animals; Blood Glucose; Body Temperature; Brain; Chickens; Fasting; Heat-Shock Proteins; Heat-Shock Response; Hypothermia; Male; Naphthalenes; Neuropeptide Y; Pyrimidines; Receptors, Neuropeptide Y

Siberian hamsters (Phodopus sungorus) undergo bouts of daily torpor during which body temperature decreases by as much as 20 degrees C and provides a significant savings in energy expenditure. Natural torpor in this species is normally triggered by winterlike photoperiods and low ambient temperatures. Intracerebroventricular injection of neuropeptide Y (NPY) reliably induces torporlike hypothermia that resembles natural torpor. NPY-induced torporlike hypothermia is also produced by intracerebroventricular injections of an NPY Y1 receptor agonist but not by injections of an NPY Y5 receptor agonist. In this research, groups of cold-acclimated Siberian hamsters were either coinjected with a Y1 receptor antagonist (1229U91) and NPY or were coinjected with a Y5 receptor antagonist (CGP71683) and NPY in counterbalanced designs. Paired vehicle + NPY induced torporlike hypothermia in 92% of the hamsters, whereas coinjection of Y1 antagonist + NPY induced torporlike hypothermia in 4% of the hamsters. In contrast, paired injections of vehicle + NPY and Y5 antagonist + NPY induced torporlike hypothermia in 100% and 91% of the hamsters, respectively. Although Y5 antagonist treatment alone had no effect on body temperature, Y1 antagonist injections produced hyperthermia compared with controls. Both Y1 antagonist and Y5 antagonist injections significantly reduced food ingestion 24 h after treatment. We conclude that activation of NPY 1 receptors is both sufficient and necessary for NPY-induced torporlike hypothermia.

Topics: Acclimatization; Animals; Body Temperature; Body Temperature Regulation; Cold Temperature; Cricetinae; Eating; Female; Hibernation; Hypothermia; Naphthalenes; Neuropeptide Y; Peptides, Cyclic; Phodopus; Photoperiod; Pyrimidines; Receptors, Neuropeptide Y