A theoretical consideration of the means whereby the mammalian core temperature is defended at a null zone.

The neural process by which it is generally supposed that the stability of the body temperature of mammals is achieved has long been sought, but it remains unresolved. One hypothesis is that, as with many engineered physical systems, there is a stable reference signal with which a signal representative of body temperature is compared. Another hypothesis is that the differing coefficients of two signals that vary with temperature changes provide the set-level determinant. These could be the activities of the "cold" and "warm" sensors in response to temperature changes. Reciprocal crossing inhibition between the cold sensor to heat production effector pathways and the warm sensor to heat loss effector pathways through the central nervous system is a likely occurrence, and it could create the null-point temperature at which neither heat production nor heat loss effectors are active. This null point would be, seemingly, the set point at which body temperature is regulated. Neither hypothesis has been validated unequivocally. Students should be aware of this uncertainty about the physiological basis of homeothermy and, indeed, of homeostasis more generally. Perhaps we should be looking for a general principle that underlies the many physical and chemical stabilities of the internal environment, rather than considering them as quite separate accomplishments.