| Abstract | The stress inoculation hypothesis presupposes that brief intermittent
stress exposure early in life induces the development of
subsequent stress resistance in human and nonhuman primates.
Rodent studies, however, suggest a role for maternal care rather
than stress exposure per se (i.e., the maternal mediation hypothesis).
To investigate these two hypotheses, we examined maternal
care and the development of stress resistance after exposure to
brief intermittent infant stress (IS), mother-infant stress (MIS), or
no stress (NS) protocols administered to 30 monkeys between
postnatal weeks 17 and 27. Unlike rodents, the IS condition did not
permanently increase primate maternal care, nor did measures of
total maternal care predict subsequent offspring hypothalamic-
pituitary-adrenal-axis responsivity. Although MIS infants received
less maternal care than IS and NS infants, both IS and MIS monkeys
developed subsequent stress resistance. These findings indicate
that rearing differences in the development of stress resistance are
more closely related to differences in prior stress exposure than to
differences in maternal care. A second experiment confirmed this
conclusion in a different cohort of 25 monkeys exposed as infants
to high foraging-demand (HFD) or low foraging-demand (LFD)
conditions. HFD infants exhibited intermittent elevations in cortisol
levels and received less maternal care than LFD infants. In
keeping with a key prediction of the stress inoculation hypothesis,
HFD males responded to stress in adulthood with diminished
hypothalamic-pituitary-adrenal-axis activation compared with
LFD males. Results from both experiments demonstrate that stress
inoculation, rather than high levels of maternal care, promotes the
development of primate stress resistance.
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