Thermoreception, thermoregulation and the early thermal environment

Abstract

Previous investigations1,2 have shown that the capacity of rats and rabbits reared at an elevated environmental temperature to thermoregulate in the cold is impaired. This impairment appears permanent and is associated with other thermoregulatory dysfunction (altered febrile response and altered response to intrahypothalamic noradrenaline injection). The present study investigated the role of the thermal environment in the development of thermoregulatory function by studying the performance of the intact thermoregulatory system and components thereof at different levels of processing of thermal information (thermoreceptive, early integrative and effector levels). The present study confirmed the impaired capacity of heat-reared rats to maintain colonic temperature in the cold and future indicated that this was likely to be attributable to active rather than passive components of the thermoregulatory system. Exposure to an environmental temperature of 20°C for 20 days was able to prevent thermoregulatory dysfunction (as assessed by intrahypothalamic noradrenaline injection) if it occurred after about 14 days of age. Exposure to 20°C was progressively less effective in averting thermoregulatory dysfunction after about 60-80 days of age. The experimental design identified these effects as being of environmental rather than genetic origin. Thermal information processing at the level of the caudal trigeminal nucleus resembled that described at thermoreceptors. The static and dynamic responses of thermoreceptive neurones at this level were quantified and found not to differ between 20°C – and 30°C-reared rats. The distribution of facial thermal receptive fields and the projections of these at the caudal trigeminal nucleus were mapped and also found not to differ. Thermal information originating from truncal skin was intercepted at a midline midbrain level. Data presented here suggested that the sites at which this thermal information could be intercepted included but probably were not restricted to the raphe nuclci. Both warm- and cold-responsive units were present at the midbrain. The abundance of thermoresponsive units was the same in 20°C- and 30°C-reared rat as was the ratio of warm:cold-responsive units. The stimulus configurations by which responses of midbrain thermoresponsive units could be characterised were more complex than at the caudal trigeminal nuclcus. Thermal responses were principally static with little response to temperature change. The pooled static responses of warm- and cold-responsive units over the 5-45°C range were the same in 20°C- and 30°C-reared rats. The cutaneous receptive fields at the midbrain level were diffuse, covering most of the truncal surface. There was an almost universal and consistent interaction with noxious input at midbrain thermoresponsive units. Warm-responsive units were inhibited by simultaneous noxious stimulation at almost any body site while the activity of cold-responsive units was augmented by such stimulation. At the thermoeffector level, noradrenaline-induced thermogenesis was equal in 20°C- and 30°C- reared rats. Heat-rearing was not observed to produce identifiable effects on the peripheral processing of thermal information, either at the afferent or efferent limbs of the thermoregulatory system. Heat-rearing does however produce changes in thermophysiological responses that are primarily mediated via a central mechanism (responses to intrahypothalamic noradrenaline, febrile response). It is therefore surmised that alterations in thermoregulatory function following heat-rearing are attributable to changes in central rather than peripheral processing of thermal information. 1 Cooper et al., (1980) J Physiol [ Lond ] 303: 165-172 2 Ferguson et al., (1981) Can J Physiol Pharmacol 59: 91-95