If one were to go out in summer and measure the 
of some property of a
cold-blooded animal one might infer that in winter that process will come to a
complete standstill. Returning in winter to repeat the measurement, however,
it may be found that the process is proceeding at the same rate as it did in
summer. Many biological processes display adaptation to temperature, coping
with seasonal changes and different latitudes. How?
As temperature goes down, the primary thing to avoid or cope with is ice crystal formation -- the crystals can cause mechanical damage to the cell membranes, and can have drastic effects on the vital osmotic and liquid balances as liquid water is removed. There are many wonderful ways in which this is achieved (eg. through supercooling [6, Chap. 21 ,]). Of particular interest is the use of antifreeze substances; it appears that these can also prevent low-temperature changes in protein structure. In this way, important enzymes may be maintained in the active state even at low temperatures, partly escaping from the Arrhenius equation.
`Acclimation depends on exploitation of the accelerations and maintenance of the independence of the limitations of the Arrhenius equation.' [6, Chap. 37,]. Inspection of the change in the rate-temperature curve before and after acclimation indicates that one, or most commonly both, of the following is responsible: (1) `altered enzyme activity due to changes in concentration, pH, water activity, or relation among enzymes'; (2) `a change in activation energy due to alteration of enzyme protein, a cofactor, or shift to alternate pathways.' [6, Chap. 37,].
Thus, in response to a temperature change, the biochemical reaction pathway responsible for a particular function may be altered in mechanism to use reactions which are suited to the new conditions. It is conceivable that this strategy could be applied to silicon: the system could be composed of many alternative low-level mechanisms for each sub-function which automatically come into play as appropriate for the current temperature.
Antifreeze (and potentially all the above mechanisms) can be regulated by (possibly seasonal) patterns of neuroendocrine activity, as well as being directly influenced by temperature. Particular physiological processes can be indicated as being concerned with compensation by identifying temperature-dependent changes in the specific enzymes associated with them. Acetylcholinesterase activity points to nervous tissues or processes as the site of compensation or lethal collapse. It has long been known that heat-death in some animals is due to nervous-system failure with a loss of indispensable reflexes such as cardiac and respiratory rhythm. Other studies (eg. in fish) have indicated that the nervous system is also the locus most sensitive to cold.
These observations suggest that there is a useful role for the nervous system in partially controlling low-level biochemical adaptation. In the silicon scheme, then, perhaps some high-level controller should also influence the choice of fine-grained mechanisms to be invoked by the current temperature. However, that controller itself might demand particular thermal precautions, as in the case of the nervous system. Note that, using an FPGA capable of rapid partial reconfiguration, the alternative mechanisms in the above scheme need not all be present on the silicon simultaneously: sub-circuits can be `swapped' in and out of the chip as appropriate for the current temperature. Indeed, several entire systems could be evolved, each for a different temperature range, the entire circuit being swapped to cope with a temperature change. There is a biological analogy: `The seasonal development of arthropods, particularly those with one generation per year, has usually evolved in such a way that only one specific stage is capable of hibernating successfully.' [6, Chap. 21,]. Here, the genotype specifies several different structures, only one of which behaves appropriately in low temperatures (by hibernating).