54 Motivation
animal uses a “comparator” to assess the difference between
its actual body temperature and its set point temperature and
that whenever there is a discrepancy between these values,
the system activates behaviors to remedy the discrepancy.
Santinoff (1983) provided both an eloquent review of the
neural circuitry of thermoregulation and an explanation of
homeostasis. The reader is advised to consult the work for
both a useful historical perspective and a comprehensive
analysis of the subject. Available evidence suggests that
the anterior hypothalamus (AH) and the preoptic (POA)
provide a significant contribution to the neural control of
thermoregulatory behavior in mammals. For example, body
temperature in animals with lesions to these areas has been
shown to drop sharply in cold environments (e.g., Satinoff &
Rutstein, 1970). Similarly, appropriate thermoregulatory re-
sponses are activated when this structure is either cooled or
heated (e.g., Fusco, Hardy, & Hammel, 1961), and electrical
stimulation of this region elicits prone extension (Roberts &
Mooney, 1974). Additionally, the POA and AH also contain
neurons that are sensitive to temperature change (Nakayama,
Hammel, Hardy, & Eisenman, 1963). Thus, the AH and POA
have the capacity to detect changes in temperatures; damage
to this region disrupts thermoregulation; and stimulation of
this region elicits appropriate responding. Together, these ob-
servations suggest that the AH and POA complex might be
the neural manifestation of the comparator that detects de-
viance from thermal homeostasis. However, lesions to this
complex do not disrupt some forms of behavioral thermoreg-
ulation. For example, rats with AH lesions are able to bar
press to obtain access to a warm heat lamp in a cold environ-
ment (Satinoff & Rutstein, 1970). Thus, animals with AH
lesions can both detect perturbations from their normal body
temperature and perform an appropriate response to hy-
pothermia. These and other observations argue against the
hypothesis that suggests the AH and POA are the neural locus
for the thermoregulatory comparator. Satinoff (1983) has
developed a more sophisticated theory of thermoregulation
that suggests multiple comparators linked to separate ther-
moregulatory behaviors and these units are organized in a
hierarchical manner.
The principle of homeostatic thermoregulation suggests
that regulatory responses occur whenever body temperature
deviates from the set point. This homeostatic explanation
does not require a motivational system, but we suggest that
thermoregulation does. That is, perhaps a behavioral systems
approach to thermoregulatory behavior is warranted. Let us
consider several points. First, the cost of ineffective ther-
moregulation is significant, so there is evolutionary pressure
to develop sophisticated thermoregulatory schemes. Second,
numerous animal species have adapted elaborate behavioral
strategies that assist in thermoregulation. Ectotherms rely
almost entirely on behavioral means. Other animals, such as
the rat, display an array of thermoregulatory behaviors that
could be organized on a continuum of relative heat stress. In-
deed, these behaviors seem to vary with the rat’s niche, as
neonates display a different repertoire than do adults. Third,
some responses to heat stress are incompatible with the
“homeostatic” account of thermoregulation. For example,
rats display a controlled hyperthermia response under condi-
tions of heat stress, and mammals exhibit fever when they are
infected by pathogens. These responses actively increase the
discrepancy in body temperature from the animal’s set point.
Thus, these responses are incompatible with the concept of a
homeostasis unless resetting the reference temperature is a
valid means at achieving homeostasis. Fourth, infant animals
provide the best examples of learning in relation to thermal
cues. These animals must cope with thermal challenge
in their niche. Perhaps we detect their ability to learn about
thermal cues because learning about these cues is critical to
their survival. Conceivably, many animals in many systems
can learn about thermal cues, and we have not detected them
only because the homeostatic thermoregulatory explanation
ignores the relevance of learning.
In summary, thermoregulation is crucial to survival in per-
haps every niche, and many behavioral responses have been
developed to cope with the problem. Given the cost of poor
thermoregulation and the propensity for animals to learn and
adapt, we propose that the study of thermoregulatory behav-
ior may profit by adopting a behavior systems approach.
CONCLUSIONS
We began this chapter by suggesting that motivation accounts
for that proportion of the variation in behavior not accounted
for by learned and genetic influences. Why is it that an animal
in the same environment presented with the same food will
eat on one occasion and not on another? Given that genetic
influences have been held constant and that no new informa-
tion has been learned about the food or the environment, this
variation must be due to changes in motivation manifested
through changes in behavior. The challenge with defining
motivation is to avoid merely redescribing the behavior in
new and empirically intractable terms. The method we have
suggested for avoiding this problem is to specify the environ-
mental cause and behavioral effect of any changes in the
hypothesized motivational construct. By defining these
antecedents and consequences in terms of the ecological and