The central control of shivering and non‐shivering thermogenesis in the rat.

Abstract

SUMMARY1. To test whether the preoptic area controls only non-shivering and the spinal cord only shivering thermogenesis, ten rats were chronically implanted with a preoptic and a spinal cord thermode each. The following were then studied: (a) the effect of propranolol (8 mg/kg. hr) on the metabolic response to cooling the preoptic area, and the spinal cord, (b) the effect of exogenous noradrenaline (0.5 mg/kg) on the metabolic response to cooling the preoptic area, and the spinal cord, and (c) the effect of warming the preoptic area on the metabolic response to cooling the spinal cord, and vice versa.2. Administration of propranolol inhibited the metabolic response to cooling each of the thermosensitive areas, but the response to cooling the preoptic area was more strongly inhibited than that to cooling the spinal cord.3. Administration of exogenous noradrenaline did not prevent the metabolic response to cooling either the preoptic area or the spinal cord.4. Warming the spinal cord completely inhibited the metabolic response to cooling the preoptic area, and warming the preoptic area fully inhibited the metabolic response to cooling the spinal cord.5. It is concluded that exogenous noradrenaline underestimates the capacity for non-shivering thermogenesis, and that both thermosensitive areas can control both forms ofthermogenesis, but that the preoptic area threshold of non-shivering thermogenesis is probably lower than that of shivering, while the spinal cord threshold of shivering is probably lower than that of non-shivering thermogenesis.

Central efferent pathways for cold‐defensive and febrile shivering

“…This observation is consistent with the possibility that the threshold skin temperature to trigger a shivering response is lower than those required to trigger BAT thermogenesis and tachycardia. In this case, the different neuronal populations in the POA, DMH and rRPa that mediate shivering, non‐shivering BAT thermogenesis and cardiovascular responses would exhibit different skin temperature thresholds for the alteration of their discharge, consistent with similar conclusions drawn from experiments with centrally positioned thermodes (Banet et al 1978). In this regard, we cannot eliminate the possibility that the magnitude of the differences in thermal thresholds for the activation of different thermal effectors may be influenced by anaesthesia.…”

Identification of Sympathetic Premotor Neurons in Medullary Raphe Regions Mediating Fever and Other Thermoregulatory Functions

“…Thus, PGE 2 is considered to act on the EP3 receptor of POA neurons and trigger fever. The POA is also known as one of the major central thermosensitive sites to monitor deep body temperature: cooling of this region causes nonshivering thermogenesis (Banet et al, 1978;Imai-Matsumura et al, 1984), possibly as a result of suppression of warmsensitive neurons (Chen et al, 1998).…”

Medullary Raphe Neurons Facilitate Brown Adipose Tissue Activation

“…Under this model, the spinal cord is the most basic site of thermoregulatory integration but can only defend a relatively wide (several degrees) thermoneutral zone, and descending modulation from the brainstem and hypothalamus progressively narrows the thermoneutral range. Indeed, the spinal cord maintains body temperature, but within a large thermoneutral zone (Simon, 1974;Banet et al, 1978). Medullary raphe lesions result in alterations of the thermoneutral zone (Szelenyi and Hinckel, 1987).…”