6.3 Metabolic regulation and the midbrain
As you found in the last section, the physiological evidence points to the likelihood that different components of regulation may be regulated separately. The hypothalamus, which appears to be central to the depression and recovery of body temperature during entry to torpor and arousal, is not the only player in the control of metabolic processes underlying non-behavioural thermogenesis. In many respects, the initiation of thermogenesis is the prime event in the reactivation of a cold body: the control mechanism which stands at the point of energy balance between dormancy and coma or even death. Centres of the brain involved in this process are likely to be efficiently protected from cooling to a critical temperature, beyond which electrical conduction and synaptic trans-mission are impossible. We do not yet know how such protection is possible in animals in hibernation, but it is clear that there is no single region of the brain with a monopoly on control of NST. The ventromedial hypothalamic nucleus is the major centre of the forebrain which stimulates the oxidation of fat in BAT as indicated by thermography studies on interscapular temperature (see Figure 21). But there is evidence that the operation of central activation mechanisms is balanced by regions that inhibit thermogenesis. Figure 39 (Hashimoto et al, 2002) shows that in a small region of the midbrain connected to the hypothalamus, electrical stimulation suppresses, whereas an injection of an anaesthetic increases T b.
It was once believed that arousal from torpor was initiated by an increase in T b, a process which was ‘paid for’ by a period of intense feeding to generate metabolic energy. The presence of an elaborate interplay between activation and inhibition of NST underlines the fact that considerable accuracy in thermogenic controls can exist for an animal within its existing limited energy budget during torpor. Such controls could not only make possible the kind of very rapid adjustments seen in Figure 27, but also contribute to the mechanisms that maintain a safe minimum BMR within the key regions of the brain.