Central NPY‐Y5 sub‐receptor partially functions as a mediator of NPY‐induced hypothermia and affords thermotolerance in heat‐exposed fasted chicks

摘要

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 style="fixed-case">HSP‐70 and ‐90, as well as of style="fixed-case">NPYSRs‐Y5, ‐Y6, and ‐Y7, but not ‐Y1, ‐Y2, and ‐Y4, under style="fixed-case">CT and style="fixed-case">HT. A coinjection of an style="fixed-case">NPYSR‐Y5 antagonist ( style="fixed-case">CGP71683) and style="fixed-case">NPY (375 pmol) attenuated the style="fixed-case">NPY‐induced hypothermia. Furthermore, central style="fixed-case">NPY decreased plasma glucose and triacylglycerol under style="fixed-case">CT and style="fixed-case">HT and kept plasma corticosterone and epinephrine lower under style="fixed-case">HT. style="fixed-case">NPY increased plasma taurine and anserine concentrations. In conclusion, brain style="fixed-case">NPYSR‐Y5 partially afforded protective thermotolerance in heat‐exposed fasted chicks. The style="fixed-case">NPY‐mediated reduction in plasma glucose and stress hormone levels and the increase in free amino acids in plasma further suggest that style="fixed-case">NPY might potentially play a role in minimizing heat stress in fasted chicks.