no specific mention of rats. There has no doubt 
been a loss of this behavior in the domestication of 
the Norway rat just as we have noted general 
aggressiveness to decline in the Wistar Institute 
breeding of wild Norway rats. Wiesner and 
S heard (69) make no mention of aggressive actions 
by the females in their extensive study of retrieving 
of young. They used Wistar albino rats. I have 
also noted that parturient females of this strain fail 
to show any aggressive action. However, Fischer 
strain rats do exhibit considerable aggressiveness 
toward an observer who places his hand in with 
recently born young. Even so, I believe that we 
are justified in concluding a general reduction in 
aggressiveness, including that associated with 
lactation, as a result of domestication. 
6 . Inhibition of Growth by Stressful Condi- 
tions 
Results from the study of the rats in the Towson 
colony showed that in a general way rate of growth 
and level of adult weight were inversely porpor- 
tional to the degree of social disturbance and in- 
stability of interindividual relationships. This 
conclusion must stand as an unsubstantiated in- 
ference because I have no quantitative proof that 
caloric intake was not reduced among rats of low 
social status. However, qualitative observations 
indicated that all rats obtained sufficient food for 
optimum growth. If they did, there still remains 
the question: could the differential experiences of 
rats in a free-ranging social milieu be logicallv 
expected to produce physiological changes culmi- 
nating in differential patterns of growth. 
The theoretical basis for growth inhibition from 
the indirect effect of external events is that of 
Selye’s (77, 18) “general-adaptation syndrome.” 
Through undefined physiological routes, pre- 
sumably of several kinds, signals reach the pituitary 
causing release of ACTH and other conditioning 
hormones. These stimulate the adrenal cortex 
to produce an array of corticoid hormones. It is 
not my intent to restate the manifold known or 
conjectured physiological effects of these corticoids. 
Suffice it to say that beyond certain specific effects, 
they produce a regular sequence of changes, re- 
gardless of a wide range of different kinds of dele- 
terious external conditions, which act as stressors on 
the organism. In the continued presence of a 
stressor condition there is an initial “alarm re- 
action” in which among other changes there is a 
decrement in lipids in the adrenal cortex. There 
follows a “stage of resistance” in which adaptations 
to the threat posed by the stressor is at an optimum 
and lipids accumulate in the adrenal cortex. If 
the stressor continues to act, and at a level imposing 
greater demands on the organism than that to 
which it is able to adjust, there follows a terminal 
“stage of exhaustion,” during which there is again 
a decrease of lipids in the adrenal cortex. Both 
the initial and terminal stages are catabolic and 
generally characterized by hypoglycemia, gastro- 
intestinal erosion, hemoconcentration, and lower- 
ing of body temperature, metabolic rate, tissue 
proteins as well as calcium and phosphates, and of 
resistance to disease, and an increase in the urine 
of sulfates, phosphates, calcium, potassium, non- 
protein nitrogen, and creatine. Just the reverse 
characterizes the anabolic stage of resistance. Re- 
tardation of growth might be anticipated whenever 
the individual is in a chronic sub-lethal stage of 
exhaustion characterized by a catabolic imbalance 
which counteracts the effects of simultaneous re- 
lease of the growth promoting hormone (STH) 
from the pituitary. 
Willier [p. 602, (70)] succinctly summarizes this 
antagonistic relationship: “. . . both the growth and 
the adrenal cortical hormones alter metabolic 
processes but in the opposite directions. The growth 
hormone seems to have the property of promoting 
protein synthesis and retention, and as a conse- 
quence promotes bodily growth. The aclrenal 
cortical hormones, on the other hand, owing to 
their capacity to accelerate the catabolic phases of 
protein metabolism, have a retarding effect upon 
rats.” Willier is apparently referring only to the 
glucocorticoids (A-Cs) produced by the adrenal 
cortex. According to Selye (18) ACTH, under 
normal conditions, stimulates the adrenal much 
more effectively to secrete glucocoricoids than 
mineralocorticoids (P-Cs). The latter actually 
enhances the effect of the growth hormone, for as 
Gaunt et al (77) have shown, injections of desoxy- 
corticosterone (DCA) actually promote more 
rapid growth. However, continued administration 
of ACTH or cortisone (77, 72) result in retarded 
growth. 
Reference has already been made (pp. 260 to 261 ) 
to the work of Rosvold and his associates who 
showed that chronic electroconvulsive shocks to 
rats in a situation permissive of conditioning of this 
experience produced alterations of adrenal function 
consistent with those culminating in those physio- 
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