W8Lupienetal.2009Effectsofstressthroughoutthelifespanonthebrainbehaviourandcognition.pdf

Every day, parents observe the growing behavioural
repertoires of their infants and young children, and
the corresponding changes in cognitive and emotional
functions. These changes are thought to relate to normal
brain development, particularly the development of the
hippocampus, the amygdala and the frontal lobes, and
the complex circuitry that connects these brain regions.
At the other end of the age spectrum, we observe changes
in cognition that accompany aging in our parents. These
changes are related to both normal and pathological
brain processes associated with aging.

Studies in animals and humans have shown that
during both early childhood and old age the brain
is particularly sensitive to stress, probably because it
undergoes such important changes during these periods.
Furthermore, research now relates exposure to early-life
stress with increased reactivity to stress and cognitive
deficits in adulthood, indicating that the effects of stress
at different periods of life interact.

Stress triggers the activation of the hypothalamus-
pituitary-adrenal (HPA) axis, culminating in the pro-
duction of glucocorticoids by the adrenals (FIG. 1).
Receptors for these steroids are expressed throughout
the brain; they can act as transcription factors and so
regulate gene expression. Thus, glucocorticoids can have
potentially long-lasting effects on the functioning of the
brain regions that regulate their release.

This Review describes the effects of stress during pre-
natal life, infancy, adolescence, adulthood and old age on
the brain, behaviour and cognition, using data from ani-
mal (BOX 1) and human studies. Here, we propose a model

that integrates the effects of stress across the lifespan,
along with future directions for stress research.

Prenatal stress
Animal studies. In animals, exposure to stress early in
life has ‘programming’ effects on the HPA axis and the
brain1. A single or repeated exposure of a pregnant
female to stress2 or to glucocorticoids3 increases mater-
nal glucocorticoid secretion. A portion of these gluco-
corticoids passes through the placenta to reach the fetus,
increasing fetal HPA axis activity and modifying brain
development4. In rats prenatal stress leads to long-term
increases in HPA axis activity 5. Controlling glucocor-
ticoid levels in stressed dams by adrenalectomy and
hormone replacement prevents these effects, indicating
that elevations in maternal glucocorticoids mediate the
prenatal programming of the HPA axis6.

Glucocorticoids are important for normal brain
maturation: they initiate terminal maturation, remodel
axons and dendrites and affect cell survival7; both sup-
pressed and elevated glucocorticoid levels impair brain
development and functioning. For example, admin-
istration of synthetic glucocorticoids to pregnant rats
delays the maturation of neurons, myelination, glia
and vasculature in the offspring, significantly altering
neuronal structure and synapse formation and inhibit-
ing neurogenesis4. Furthermore, juvenile and adult rats
exposed to prenatal stress have decreased numbers of
mineralocorticoid receptors (MRs) and glucocorticoid recep-
tors (GRs) in the hippocampus, possibly because of epi-
genetic effects on gene transcription8. The hippocampus

*Université de Montréal,
Mental Health Research
Centre, Fernand Seguin
Hôpital Louis‑H Lafontaine,
Montreal, Quebec, H1N 3V2,
Canada.
‡Laboratory of
Neuroendocrinology, The
Rockefeller University, 1230
York Avenue, New York,
New York 10021, USA.
§Institute of Child
Development, University of
Minnesota, Minneapolis,
Minnesota 55455, USA.
||Department of Psychiatry,
Emory University, 101
Woodruff Circle, Suite 4000,
Atlanta, Georgia 30307, USA.
Correspondence to S.J.L.
e‑mail: sonia.lupien@
umontreal.ca
doi:10.1038/nrn2639
Published online 29 April 2009

Programming
When an environmental factor
that acts during a sensitive
developmental period affects
the structure and function of
tissues, leading to effects that
persist throughout life.

Effects of stress throughout
the lifespan on the brain,
behaviour and cognition
Sonia J. Lupien*, Bruce S. McEwen‡, Megan R. Gunnar § and Christine Heim||

Abstract | Chronic exposure to stress hormones, whether it occurs during the prenatal
period, infancy, childhood, adolescence, adulthood or aging, has an impact on brain
structures involved in cognition and mental health. However, the specific effects on the
brain, behaviour and cognition emerge as a function of the timing and the duration of
the exposure, and some also depend on the interaction between gene effects and previous
exposure to environmental adversity. Advances in animal and human studies have made it
possible to synthesize these findings, and in this Review a model is developed to explain why
different dis s emerge in individuals exposed to stress at different times in their lives.

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Nature Reviews | Neuroscience

Hippocampus

Hypothalamus

Amygdala

CRH
AVP

ACTH

Glucocorticoids

Adrenal cortex

Anterior pituitary

Frontal cortex

GRs

GRs

GRs

MRs and
GRs

Mineralocorticoid receptor
A receptor that is activated by
mineralocorticoids, such as
aldosterone and deoxycorti-
costerone, as well as
glucocorticoids, such as
cortisol and cortisone. It also
responds to progestins.

Glucocorticoid receptor
A receptor that is activated by
cortisol, corticosterone and
other glucocorticoids and is
expressed in almost every cell
in the body. It regulates genes
controlling development,
metabolism and the immune
response.

inhibits HPA axis activity (FIG. 1), and a prenatal stress-
induced reduction in hippocampal MRs and GRs could
decrease this inhibition, with a resulting increase in basal
and/or stress-induced glucocorticoid secretion. In rhe-
sus monkeys, prenatal treatment with the synthetic GR
agonist dexamethasone causes a dose-dependent degen-
eration of hippocampal neurons, leading to a reduced
hippocampal volume at 20 months of age9.

Effects on other brain regions are also apparent.
Rats exposed to stress during the last week of gestation
have significantly decreased dendritic spine density in
the anterior cingulate gyrus and orbitofrontal cortex10.
Furthermore, prenatal exposure to glucocorticoids leads
to increased adult corticotropin-releasing hormone
(CRH) levels in the central nucleus of the amygdala, a
key region in the regulation of fear and anxiety11.

Exposure to prenatal stress has three major effects
on adult behaviour: learning impairments, especially
in aging rats12; enhanced sensitivity to drugs of abuse13;
and increases in anxiety- and depression-related behav-
iours14. The impaired learning is thought to result from
the effects of prenatal stress on hippocampal function15,
whereas the effects on anxiety are thought to be medi-
ated by prenatal stress-induced increases in CRH in the
amygdala11. Prenatal glucocorticoid exposure affects
the developing dopaminergic system, which is involved
in reward- or drug-seeking behaviour16, and it has been

suggested that the increased sensitivity to drugs of abuse
is related to the interaction between prenatal stress,
glucocorticoids and dopaminergic neurons16.

Human studies. In agreement with animal data, findings
from retrospective studies on children whose mothers
experienced psychological stress or adverse events or
received exogenous glucocorticoids during pregnancy
suggest that there are long-term neurodevelopmental
effects17. First, maternal stress or anxiety18, depression19
and glucocorticoid treatment during pregnancy17 have
been linked with lower birthweight or smaller size (for
gestational age) of the baby. More importantly, mater-
nal stress, depression and anxiety have been associated
with increased basal HPA axis activity in the offspring
at different ages, including 6 months20, 5 years21 and
10 years22.

Disturbances in child development (both neurologi-
cal and cognitive) and behaviour have been associated
with maternal stress23 and maternal depression dur-
ing pregnancy 24, and with fetal exposure to exogenous
gluco corticoids in early pregnancy 25. These behavioural
alterations include unsociable and inconsiderate behav-
iours, attention deficit hyperactivity dis and sleep
disturbances as well as some psychiatric dis s,
including depressive symptoms, drug abuse and mood
and anxiety dis s. Very few studies have measured

Figure 1 | The stress system. When the brain detects a
threat, a coordinated physiological response involving
autonomic, neuroendocrine, metabolic and immune
system components is activated. A key system in the
stress response that has been extensively studied is the
hypothalamus-pituitary-adrenal (HPA) axis. Neurons in
the medial parvocellular region of the paraventricular
nucleus of the hypothalamus release corticotropin-
releasing hormone (CRH) and arginine vasopressin (AVP).
This triggers the subsequent secretion of adrenocortico-
tropic hormone (ACTH) from the pituitary gland, leading
to the production of glucocorticoids by the adrenal
cortex. In addition, the adrenal medulla releases
catecholamines (adrenaline and noradrenaline) (not
shown). The responsiveness of the HPA axis to stress is in
part determined by the ability of glucocorticoids to
regulate ACTH and CRH release by binding to two
corticosteroid receptors, the glucocorticoid receptor
(GR) and the mineralocorticoid receptor (MR). Following
activation of the system, and once the perceived stressor
has subsided, feedback loops are triggered at various
levels of the system (that is, from the adrenal gland to the
hypothalamus and other brain regions such as the
hippocampus and the frontal cortex) in to shut the
HPA axis down and return to a set homeostatic point. By
contrast, the amygdala, which is involved in fear
processing142, activates the HPA axis in to set in
motion the stress response that is necessary to deal with
the challenge. Not shown are the other major systems
and factors that respond to stress, including the
autonomic nervous system, the inflammatory cytokines
and the metabolic hormones. All of these are affected by
HPA activity and, in turn, affect HPA function, and they
are also implicated in the pathophysiological changes
that occur in response to chronic stress, from early
experiences into adult life.

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changes in the brain as a function of prenatal stress in
humans. However, a recent study showed that low birth-
weight combined with lower levels of maternal care was
associated with reduced hippocampal volume in adult-
hood26. This finding is consistent with evidence that
effects of prenatal stress in humans are often moderated
by the quality of postnatal care, which in turn is consist-
ent with the protracted postnatal development of the
human brain.

Postnatal stress
Animal studies. Although in rodents the postnatal
period is relatively hyporesponsive to stress (BOX 2), one
of the most potent stressors for pups is separation from
the dam. long separation periods (3 h or more each day)
activate the pups’ HPA axis, as evidenced by increased
plasma levels of adrenocorticotropic hormone and
glucocorticoids27. Protracted maternal separation also
reduces pituitary CRH binding sites28, and low levels of
maternal care reduce GR levels in the hippocampus29.

The effects of maternal deprivation extend beyond
the HPA axis. Early prolonged maternal separation in
rats increases the density of CRH binding sites in the
prefrontal cortex, amygdala, hypothalamus, hippo-
campus and cerebellum, as measured post-infancy28. In
the hippocampus CRH mediates stress-related loss of
branches and spines30, and in the amygdala and hypotha-
lamus elevated CRH levels are associated with increased
anxiety and HPA axis activity, respectively31. Thus, the
increase in CRH-binding sites induced by maternal sep-
aration might have negative effects over time. The long-
term effects of prolonged separation depend on the age

of the pup and the duration of the deprivation, with the
effects noted above generally being greater when these
separations occur earlier in infancy and last for longer
durations32.

Although the rodent work provides a rich frame-
work for conceptualizing the impact of early-life stress,
the fact that the rodent brain is much less developed at
birth than the primate brain makes translation of the
findings to humans somewhat challenging (BOX 3). non-
human primates have more human-like brain matura-
tion at birth and patterns of parent–offspring relations,
and so provide an important bridge in the translation of
the rodent findings. Studies in monkeys have shown that
repeated, unpredictable separations from the mother33,
unpredictable maternal feedings34 or spontaneous mater-
nal abusive behaviour35 increases CRH concentrations
in the cerebrospinal fluid and alters the diurnal activity
of the HPA axis for months or even years after the period of
adversity: cortisol levels are lower than normal early in
the morning (around wake-up) and slightly higher than
normal later in the day, an effect that seems to reverse
over time in the absence of continued, ongoing psy-
chosocial stress35. These diurnal effects have not been
noted in rodents, but the effects on higher brain regions
seem to be comparable to the rodent findings and
include heightened fear behaviour36, exaggerated startle
responses33, hippocampal changes such as an increase in
the intensity of non-phosphorylated neurofilament pro-
tein immunoreactivity in the dentate gyrus granule cell
layer37, and atypical development of prefrontal regions
involved in emotion and behaviour control38.

Human studies. A human equivalent of the rodent
maternal separation paradigms might be studies of
children who attend full-day, out-of-home day care
centres. Studies have reported that glucocorticoid levels
rise in these children over the day, more so in toddlers
than in older preschool-aged children39,40. However, it is
important to note that the elevated glucocorticoid levels
observed are less pronounced than those observed in
rodents and monkeys exposed to maternal separation.
Moreover, although age accounts for most of the varia-
tion in the rise in glucocorticoid levels by late afternoon,
the quality of care is also important, with less supportive
care producing larger increases, especially for children
who are more emotionally negative and behaviour-
ally disorganized39. So far, there is no evidence that the
elevated glucocorticoid levels associated with being in
day care affect development; however, children who are
exposed to poor care for long hours early in develop-
ment have an increased risk of behaviour problems later
in development41.

Parent–child interactions and the psychological state
of the mother also influence the child’s HPA axis activity.
Beginning early in the first year, when the HPA system
of the infant is quite labile, sensitive parenting is associ-
ated with either smaller increases in or less prolonged
activations of the HPA axis to everyday perturbations42.
Maternal depression often interferes with sensitive and
supportive care of the infant and young child; there is
increasing evidence that offspring of depressed mothers,

Box 1 | Models to study stress in animals and humans

The hypothalamus-pituitary-adrenal axis can be activated by a wide variety of stressors.
Some of the most potent are psychological or processive stressors (that is, stressors that
involve higher- sensory cognitive processing), as opposed to physiological or
systemic stressors. Many psychological stressors are anticipatory in nature — that is,
they are based on expectation as the result of learning and memory (for example,
conditioned stimuli in animals and the anticipation of threats, real or implied, in humans)
or on species-specific predispositions (for example, avoidance of open space in
rodents or the threat of social rejection and negative social evaluations in humans).

Animal studies allow the development of experimental protocols in which animals
are submitted to acute and/or chronic stress and the resulting effects on brain and
behaviour are studied. Experimental stressful ‘early-life’ manipulations in animals can
be broadly split into prenatal and postnatal manipulations. Prenatal manipulations
involve maternal stress, exposing the mother to synthetic glucocorticoids or maternal
nutrient restriction. Postnatal manipulations include depriving the animal of
maternal contact, modifying maternal behaviour and exposing the animal to synthetic
glucocorticoids. In these protocols, the cause–effects relationship between stress and
its impact on the brain can be demonstrated. By contrast, and because of ethical issues,
the cause–effects impact of stress on the brain cannot be studied in humans, and most
human studies are correlational by nature. However, there are some ‘experiments of
nature’ that can be used to inform scientists about the effects of chronic exposure to
early adversity on brain development and of adulthood and late-life stress effects on
the brain. Intrauterine under-growth and low birth weight are considered indices of
prenatal stress (including malnutrition) in humans. In terms of postnatal stress, low
socio-economic status, maltreatment and war are considered adverse events. In adults
and older adults, studies of chronic caregivers (spouses of patients with brain
degenerative dis s, parents of chronically sick children and health-care
professionals) provide a human model of the impact of chronic stress on the brain,
behaviour and cognition.

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especially those who were clinically depressed in the
child’s early years, are at risk of heightened activity of
the HPA axis43 or of developing depression during ado-
lescence (controlling for maternal depression during
adolescence)44. However, it should be noted that it can
be difficult to exclude potentially confounding genetic
factors in such studies. Furthermore, preschool-aged
children of depressed mothers exhibit electroencephalo-
graphic alterations in frontal lobe activity that corre-
late with diminished empathy and other behavioural
problems45.

In contrast to findings of elevated glucocorticoid lev-
els in conditions of low parental care, studies in human
children exposed to severe deprivation (for example,
in orphanages or other institutions), neglect or abuse
report lower basal levels of glucocorticoids, similar to
what has been observed in primates39. one proposed
mechanism for the development of hypocortisolism is
downregulation of the HPA axis at the level of the pitui-
tary in response to chronic CRH drive from the hypoth-
alamus46, whereas a second possible mechanism is target
tissue hypersensitivity to glucocorticoids47. Importantly,
this hypocortisolism in humans in response to severe
stress may not be permanent: sensitive and supportive
care of fostered children normalizes their basal gluco-
corticoid levels after only 10 weeks48. Another impor-
tant finding comes from a recent study which showed
that exposure to early adversity is associated with epi-
genetic regulation of the GR receptor, as measured in the
post-mortem brains of suicide victims49.

Stress in adolescence
Animal studies. In rodents the period of adolescence has
three stages: a prepubescent or early adolescent period
from day 21 to 34, a mid-adolescent period from day
34 to 46 and a late adolescent period from day 46 to 59

(ReF. 50). In humans, adolescence is often considered
to demarcate the period of sexual maturation (that is,
starting with menarche in girls).

Although adolescence is a time of significant brain
development, particularly in the frontal lobe51, there has
been relatively little research on stress during this period
in rodents. In adolescent rodents, HPA function is char-
acterized by a prolonged activation in response to stres-
sors compared with adulthood. Moreover, prepubertal
rats have a delayed rise of glucocorticoid levels and
prolonged glucocorticoid release in response to several
types of stressors compared with adult rats52, owing to
incomplete maturation of negative-feedback systems53.

In contrast to adult rats, which show a habituation of
the stress response with repeated exposure to the same
stressor 54, juvenile rats have a potentiated release of
adrenocorticotropic hormone and glucocorticoids after
repeated exposure to stress55, suggesting that the HPA
axis responses to acute and chronic stress depend on
the developmental stage of the animal. Compared with
exposure to stress in adulthood alone, exposure to stress
as both a juvenile and an adult increases basal anxiety
levels in the adult 56. Moreover, exposure to juvenile
stress results in greater HPA axis activation than a dou-
ble exposure to stress during adulthood56, and this effect
is long-lasting. These results suggest that repeated stress
in adolescence leads to greater exposure of the brain to
glucocorticoids than similar experiences in adulthood.

The fact that the adolescent brain undergoes vigor-
ous maturation and the fact that, in rats, the hippocam-
pus continues to grow until adulthood suggest that the
adolescent brain may be more susceptible to stressors
and the concomitant exposure to high levels of gluco-
corticoids than the adult brain. Consistent with this
hypothesis are findings that increased glucocorticoid
levels before but not after puberty alter the expression of
genes for nMDA (N-methyl-d-aspartate) receptor sub-
units in the hippocampus57. In addition, chronic, vari-
able stress during the peripubertal juvenile period results
in reduced hippocampal volume in adulthood, which
is accompanied by impairments in Morris water maze
navigation and delayed shutdown of the HPA response
to acute stress58. These differences became evident only
in adulthood58, suggesting that stress in adolescence
reduces hippocampal growth. Finally, the effects of juve-
nile stress are long-lasting: adult rats exposed to juvenile
stress exhibit reduced exploratory behaviour and poor
avoidance learning 59. Moreover, stress in adolescence
increases susceptibility to drugs of abuse during the
adolescent period60 and in adulthood61.

Human studies. Interestingly, studies in human adoles-
cents also suggest that the adolescent period is associ-
ated with heightened basal and stress-induced activity
of the HPA axis62. This could be related to the dramatic
changes in sex steroid levels during this period, as these
steroids influence HPA axis activity50. However, studies
of stress in adolescent rats cannot be translated directly
to humans because the brain areas that are undergoing
development during adolescence differ between rats and
humans: although the rodent hippocampus continues to

Box 2 | The stress hyporesponsive period: from animals to humans

Despite there being clear evidence that corticotropin-releasing hormone-containing
neurons are present in the fetal rat139, in rodents noxious stimuli evoke only a
subnormal hypothalamus-pituitary-adrenal (HPA) axis response during the first 2 weeks
of life140. During this so-called stress hyporesponsive period (SHRP), baseline plasma
glucocorticoid levels are lower than normal and are only minimally increased by
exposure to a noxious stressor140. The SHRP is due to a rapid regression of the HPA axis
after birth140 and may have evolved in rodents to protect the rapidly developing brain
from the impact of elevated glucocorticoids.

Evidence is accumulating that in children there may be a comparable hyporesponsive
period that emerges in infancy and extends throughout most of childhood141. At birth,
glucocorticoid levels increase sharply in response to various stressors, such as a
physical examination or a heel lance. However, over the course of the first year the HPA
axis becomes more insensitive to stressors. No study has assessed the exact period over
which this human SHRP may occur, but in adolescents glucocorticoid levels can
become elevated in response to a psychosocial stressor141, which suggests that the
SHRP could extend throughout childhood.

In rodents the SHRP is maintained primarily by maternal care (that is, the presence of
the dam seems to suppress HPA axis activity); indeed, maternal separation is a potent
inducer of a stress response, even during the SHRP. Similarly, in humans the apparent
hyporesponsivity of the HPA axis might reflect the fact that during the first year of life
the HPA axis comes under strong social regulation or parental buffering141. Here again,
stressors that involve a lack of parental care or social contact can induce a stress
response in children.

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develop well into adulthood, in humans it is fully devel-
oped by 2 years of age63. The frontal cortex and amygdala
continue to develop in both species, but humans have
larger ontogenic bouts of development in frontal regions
than do rodents (BOX 3).

There are indications that the adolescent human brain
might be especially sensitive to the effects of elevated
levels of glucocorticoids and, by extension, to stress.
Recent studies on the ontogeny of MR and GR expres-
sion show that GR mRnA levels in the prefrontal cortex
are high in adolescence and late adulthood compared
with in infancy, young adulthood and senescence64. This
suggests that the cognitive and emotional processes that
are regulated by these brain areas might be sensitive to
GR-mediated regulation by glucocorticoids in an age-
dependent manner. Various forms of psychopathology,
including depression and anxiety, increase in prevalence
in adolescence65,66. Periods of heightened stress often
precede the first episodes of these dis s, raising the
possibility that heightened HPA reactivity during adoles-
cence increases sensitivity to the onset of stress-related
mental dis s.

Adolescence is also a period in which the long-
lasting effects of earlier exposures to stress become evi-
dent. Adolescents who grew up in poor economic condi-
tions have higher baseline glucocorticoid levels67, as do
adolescents whose mothers were depressed in the early
postnatal period44. High early-morning glucocorticoid
levels that vary markedly from day to day during the
transition to adolescence are not associated with depres-
sive symptoms at that time, but they predict increased
risk for depression by age 16 (ReF. 44).

Although early-life stress impairs hippocampal devel-
opment in rodents, there is currently little evidence

of comparable effects in humans. Children exposed
to physical or sexual abuse early in life do not exhibit
reduced hippocampal volume (relative to whole-brain
size) as adolescents, although adults with these histo-
ries do show volume reductions68. This finding holds
even when the abused children have been selected for
chronic post-traumatic stress dis (PTSD), and even
though in some cases they exhibit overall reductions in
brain volume69. By contrast, alterations in grey matter
volume and the neuronal integrity of the frontal cortex,
and reduced size of the anterior cingulate cortex, have
been reported in adolescents exposed to early (and con-
tinued) adversity70. Together, these results suggest that in
humans the frontal cortex, which continues to develop
during adolescence, might be particularly vulnerable to
the effects of stress during adolescence. By contrast, the
hippocampus, which develops mainly in the first years
of life, might be less affected by exposure to adversity in
adolescence.

Stress in adulthood
Animal studies. Studies on adult stress in rodents have
delineated the effects of acute versus chronic stress
on brain and behaviour. The impact of acute stressors
depends on the level of glucocorticoid elevations, with
small increases resulting in enhanced hippocampus-
mediated learning and memory, and larger, prolonged
elevations impairing hippocampal function71. The
inverted-u-shaped effects of acute glucocorticoid ele-
vations might serve adaptive purposes by increasing
vigilance and learning processes during acute challenges.

The mechanism that underlies the acute bipha-
sic actions of glucocorticoids on cognition involves
the adrenergic system in the basolateral nucleus of the
amygdala. By enhancing noradrenergic function in
the amygdala, glucocorticoids have a permissive effect
on the priming of long-term potentiation in the den-
tate gyrus by the basolateral nucleus72. This modulation
of noradrenergic function by glucocorticoids has been
linked to the enhanced memory for emotional events
that occur under stress73.

Chronic stress or chronic exogenous administration
of glucocorticoids in rodents causes dendritic atrophy
in hippocampal CA3 pyramidal neurons74. However,
these changes take several weeks to …