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First published online April 17, 2009
Journal of Experimental Biology 212, 1405-1412 (2009)
Published by The Company of Biologists 2009
doi: 10.1242/jeb.024455
Effects of a short period of elevated circulating corticosterone on postnatal growth in free-living Eurasian kestrels Falco tinnunculus
1 Swiss Ornithological Institute, Luzernerstrasse 6, CH-6204 Sempach,
Switzerland
2 Zoological Museum of the University of Zurich, Winterthurerstrasse 190,
CH-8057 Zurich
* Author for correspondence (e-mail: claudia.mueller{at}vogelwarte.ch)
Accepted 12 February 2009
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Summary |
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 TOP Summary INTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONReferences |
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Key words: bone growth, corticosterone implants, feather growth, morphology, stress effects
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INTRODUCTION |
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TOPSummaryINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONReferences |
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).
Energetic restrictions or other environmental perturbations during growth and
development may provoke a trade-off between current survival and development.
Many effects of environmental factors on growth and development are
irreversible and thus often have consequences for life
(Lindström, 1999).
Glucocorticoids may play an important role in this trade-off between
maintenance and development. Across all vertebrate taxa, the activation of the
hypothalamo-pituitary-adrenal (HPA) axis, leading to a rise in
glucocorticoids, helps an animal to redirect the available energy and
behaviour from normal activities into a survival mode, to cope with the
critical situation (e.g. Wingfield et al.,
1998). Elevated glucocorticoid levels inhibit anabolic processes
including growth, suppress parts of the immune system and influence appetite
(e.g. Bray, 1993;
Sapolsky et al., 2000;
Lin et al., 2006). Thus
environmental factors may affect growth and development directly (e.g. limited
nutrients) and indirectly through glucocorticoids which may have suppressing
effects on growth and development, such as on body size, body condition,
immune system and cognitive functions (e.g.
Davison et al., 1983;
Saino et al., 2003;
Kitaysky et al., 2003;
Hull et al., 2007). Therefore,
glucocorticoids, as mediators of environmental conditions and through their
indirect effects, may be an important additional factor causing developmental
plasticity and thus, through long-term or life-long effects, shape phenotype
(Dufty et al., 2002).
The most common environmental factor affecting growth and development is
nutritional restriction (through food shortage, competition with siblings,
parasites), but disease, heat, cold and water shortage can also have an
effect. Most studies have used food restriction to investigate developmental
plasticity as a response to environmental conditions, and thereby have studied
the combined effects of both the nutrient restriction per se and
elevated glucocorticoids. Most studies available on the effects of
glucocorticoids during growth and development are from precocial species such
as quail and chicken under lab conditions (e.g.
Davison et al., 1983;
Donker and Beuving, 1989;
Hayashi et al., 1994). Studies
on the effect of glucocorticoids during growth in altricial chicks and under
natural conditions are few and focus mainly on behavioural aspects
(Kitaysky et al., 2001b;
Loiseau et al., 2008;
Wada and Breuner, 2008).
Precocial chicks forage for themselves and glucocorticoids may have effects
similar to those in adults, i.e. enhance food searching behaviour
(Astheimer et al., 1992;
Sapolsky et al., 2000).
Altricial nestlings, however, are completely dependent on their parents for
food, but also have a HPA axis responsive to stressors (e.g.
Love et al., 2003). The
function of increased glucocorticoids in altricial nestlings may be (a) to
improve energy intake by increased begging and by becoming more aggressive
towards their siblings (Kitaysky et al.,
2003) and (b) to re-allocate the available energy to the most
important processes (e.g. Sapolsky et al.,
2000; Hochberg,
2002).
The aim of this study was to investigate the effects of a temporary
increase of circulating corticosterone (the glucocorticoid in birds) on growth
in an altricial bird species, the Eurasian kestrel Falco tinnunculus,
in natural conditions in the wild. Because we artificially elevated
circulating corticosterone for a few days with implants, we could investigate
the effects of corticosterone without the confounding effects of food
restriction. In most food restriction studies, glucocorticoid levels have not
been measured and, thus, it was not known what the direct effects of food
restriction and the indirect effects of elevated glucocorticoid levels were,
while in some food restriction studies glucocorticoids were measured but the
effects on structural growth were not documented
(Kitaysky et al., 1999;
Kitaysky et al., 2001a;
Pravosudov and Kitaysky, 2006;
Strochlic and Romero,
2008).
Contrary to most studies investigating the effects of a long stress period
on postnatal development, we were interested in the effects of a short period
(2–3 days) of clearly elevated baseline corticosterone levels. We used
different growth and body condition measures in order to investigate whether
growth of skeletal elements, feathers, body mass and subcutaneous body fat
stores was affected differently by elevated corticosterone levels. Food
restriction studies demonstrated a hierarchy in resource allocation favouring
important structures, such as the nervous system and skeletal structures, at
the expense of muscles, the digestive system and fat stores
(Oyan and Anker-Nilssen, 1996;
Schew and Ricklefs, 1998;
Moe et al., 2004). However,
there are hardly any studies investigating the effects of elevated
corticosterone on various structures (including body size) and tissues in
birds; exceptions investigating internal organs include the precocial chicken
and quail (e.g. Lin et al.,
2006; Hull et al.,
2007).
We investigated the effects of elevated circulating corticosterone in the
middle of the nestling stage and were therefore able to test for compensatory
growth after the corticosterone levels returned back to normal. Food
restriction studies have shown that delays in growth may be partly or fully
compensated for through a prolongation or acceleration of growth (e.g.
Emlen et al., 1991;
Negro et al., 1994;
Bize et al., 2003;
Bize et al., 2006) possibly
with associated costs (Metcalfe and
Monaghan, 2001). Because this study was done in the wild, we
examined whether compensatory growth occurred under natural, rather than
ad libitum, food conditions. Thus our results are directly relevant
to natural populations.
In the kestrel, males are slightly smaller than females and nestlings hatch partially asynchronously. Therefore we also investigated whether elevated corticosterone levels affected growth of the smaller sex or smaller chicks differently from growth of the larger ones.
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MATERIALS AND METHODS |
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TOPSummaryINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONReferences |
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Experimental corticosterone elevation
The experiment was carried out with 109 nestlings of 13 broods in 2004 and
17 broods in 2005. There was no difference between the years in all
parameters; therefore the year was not included in the analysis.
During both breeding seasons, nest boxes were checked weekly from April onwards and before hatching (from May to June) at 4 day intervals to determine hatching date. At the age of 13 days, two randomly selected nestlings out of the four oldest within a brood were implanted with a biodegradable corticosterone implant (Innovative Research of America, Sarasota, FL, USA; 10 mg corticosterone, 7 day release) and called cort-nestlings, and the other two were implanted with a placebo pellet (placebo-nestlings). To monitor the effect of the implant on circulating corticosterone levels, we took baseline blood samples at the age of 10, 13, 16 and 21 days in all nestlings. In a subgroup of the nestlings we took an additional sample at day 14 or 15. Within 3 min of taking nestlings out of the nest box, the alar vein was punctured and about 80 µl blood was sampled with heparinized capillary tubes. Corticosterone levels did not rise significantly within 3 min as a response to capture (F=3.29, d.f.=1, P=0.071). Within 30 min, the blood was centrifuged and the plasma stored in liquid nitrogen in the field and at –20°C once in the laboratory. All methods described in this study were approved by the Cantonal committee for animal research (animal experiment permit no. 274 from the Cantonal Veterinarian Office of Baselland).
Growth and body condition measurements
Nestlings were measured at the age of 10, 13, 16, 21 and 25 days (age of
the oldest nestlings of the brood). We refrained from visiting the nests after
day 25 to avoid premature fledging. The length of the wing and of primary 8
(second longest primary) were measured to the nearest 0.5 mm. An estimate of
the skeletal hand length was obtained by subtracting the length of primary 8
from the wing length. Tarsus length was measured to the nearest 0.1 mm with
digital calipers. Body mass was determined with a spring balance to the
nearest gram. As in passerines (Kaiser,
1993), we assessed the subcutaneous fat stores at the furcula by
assigning a fat score ranging from 0 to 4 (0: no visible fat; 1: 1 mm stripe
of fat at the bottom of the furcular pit; 2: fat stripes 2–3 mm wide; 3:
furcular pit nearly covered with fat (about 75%), 4: furcular pit completely
filled with fat). Growth rates were calculated on the basis of the number of
hours between measurements and expressed as growth rates per 24 h.
From nest controls at hatching and wing length at day 10, we determined the age difference between the oldest nestlings and their siblings. Between the treated nestlings within a brood, this age difference ranged from 0 to 3 days (0 days: 56 nestlings; 1 day: 43 nestlings; 2 days: 12 nestlings; 3 days: 1 nestling). For 18% of the sampling days, we were unable to measure the nestlings on the intended day for logistical reasons and did it 1 day earlier or later. Because there was no significant effect of bringing forward or delaying measurements on growth parameters, we omitted it from the analysis.
At the age of 10 and 13 days, 3 and 0 days before the treatment, there were no significant differences between the future corticosterone and placebo groups in any of the parameters measured (data not shown, but see day 10 and 13 values in Fig. 1).
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Hormone assay
Plasma corticosterone concentration was determined using an enzyme
immunoassay. Corticosterone in 5 µl plasma and 195 µl water was
extracted with 4 ml dichloromethane, re-dissolved in phosphate buffer and
given in triplicate in the enzyme immunoassay. The dilution of the
corticosterone antibody (Chemicon, Temecula, CA, USA; cross-reactivity:
11-dehydrocorticosterone 0.35%, progesterone 0.004%, 18-OH-DOC 0.01%, cortisol
0.12%, 18-OH-B 0.02% and aldosterone 0.06%) was 1:8000. Horseradish peroxidase
(1:400,000) linked to corticosterone served as the enzyme label and ABTS
[2,2'-azino-bis(3-ethylbenzthiazoline-6-sulphonic acid)] as the
substrate. The concentration of corticosterone in plasma samples was
calculated by using a standard curve run in duplicate on each plate. Plasma
pools from chickens with two different corticosterone concentrations were
included as internal controls on each plate. If the concentration was below
the detection threshold, the determination was repeated with 10 µl plasma.
If the concentration was still below the detection threshold, the value of the
lowest detectable concentration (1 ng ml–1) was assigned.
Intra-assay variation ranged from 4.5 to 10.8% and inter-assay variation from
9.6 to 17.6%, depending on the concentration of the internal control and the
year of determination.
Sex determination
Nestlings were sexed with molecular methods by fragment analysis on
CHD1W/CHD1Z (Fridolfsson and Ellegren,
1999) using blood cells of blood samples extracted with the QIAamp
DNA extraction kit (Qiagen, Hombrechtikon, Switzerland) in 2004 and after
Kawasaki (Kawasaki, 1990) in
2005. Samples from 2004 were analysed at the Swiss Federal Institute for
Forest, Snow and Landscape Research in Birmensdorf, Switzerland and those from
2005 at the Agroscope Research Station ACW in Wädenswil, Switzerland.
Statistical analysis
Growth rates were analysed with a mixed model for repeated measurements in
Genstat 9.1 (Payne, 2003;
Thompson and Welham, 2003). In
the fixed model, the effect of the corticosterone treatment on primary, hand
and tarsus growth rate and body mass and furcular fat store increase was
examined taking into account age (in days), time of day, sex, age difference
to the oldest nestling within the brood (in days), brood size, the absolute
measure of the parameter of this individual at day 10 and hatching date
(Julian date). After the main parameters, biologically relevant interactions
between age, sex, age difference within the brood and treatment were tested.
The design of the random model was broodxage. The nestling variance
component was very small and therefore omitted from the random model.
To assess the effect of corticosterone treatment on growth rate, body size
and condition before and during the experiment and just before fledging, the
growth rates and absolute morphological measurements (primary 8, hand and
tarsus length, body mass, fat score) at day 10, 13, 16, 21 and 25 were
analysed separately in post-hoc mixed models with time of
day, sex, the age difference to the oldest nestling within the brood, brood
size, hatching date, treatment and relevant two-way interactions in the fixed
model and brood as random model. Because individuals were measured repeatedly,
significance levels were adjusted according to Bonferroni
(Sokal and Rohlf, 2000). All
model residuals were normally distributed.
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RESULTS |
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TOPSummaryINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONReferences |
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). Corticosterone treatment occurred when the growth rate of primary 8 was high and temporarily reduced it (interaction agextreatment highly significant; Table 1; Fig. 1A). Primary growth rate in cort-nestlings was significantly reduced (for statistics see Fig. 1) to 71% of the placebo-nestlings during the period of elevated circulating corticosterone (from nestling day 13 to 16; Fig. 1A). During the 5 days after treatment (day 16–21), primary growth rate was still significantly reduced to 84% of the placebo group and recovered only in the following period from day 21 to 25, when it corresponded to the placebo group again. At day 25, cort-nestlings had a significantly shorter primary (10.3 mm or 10%; Table 2; Fig. 1B) than the placebo-nestlings. At this age, primary 8 had reached about 53% of its final length.
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For both hand and tarsus, corticosterone treatment occurred during the final growth phase as shown by the strongly decreasing growth rates in placebo birds from day 10 to day 21 (Fig. 1C,E; age significant, Table 1). Corticosterone treatment temporarily reduced hand and tarsus growth significantly (interaction agextreatment significant; Fig. 1C,E). During the period of elevated circulating corticosterone (days 13–16), hand growth rate of the cort-nestlings was only 14% of the rate of the placebo group (Fig. 1C) and tarsus growth rate only 26% (Fig. 1E). After the period of high corticosterone levels (days 16–21), hand and tarsus growth rates of the cort-nestlings had recovered and were indistinguishable from those of the placebo group. At day 25, when hand growth is almost completed, cort-nestlings had a 2.8 mm or 5% shorter hand length (Table 2; Fig. 1D). In contrast to the hand, cort-nestlings still grew their tarsi from day 21 to 25 and compensated for the reduction to a certain degree, while tarsus growth was already completed in the placebo group (Fig. 1E,F). On day 25, cort-nestlings had a 1.5 mm or 4% shorter tarsus than the placebo group (Table 2; Fig. 1F).
Corticosterone treatment strongly affected body mass growth (Table 1; Fig. 1G). Body mass growth rate of the cort-nestlings was negative during the period of elevated circulating corticosterone while the placebo-nestlings gained about 9 g day–1. During the 5 days after the treatment, from day 16 to 21, the two groups had similar growth rates. From day 21 to 25, the body mass retardation of cort-nestlings was partly compensated for by growing at 265% compared with the placebo group (difference in growth rate significant). On day 25, cort-nestlings had a significantly lower body mass (by 18 g or 8.5%) than the placebo group (Table 2; Fig. 1H). At this age, adult body mass has been reached or surpassed by normally developing nestlings.
Corticosterone treatment had no overall significant effect on furcular fat score increase and placebo- and cort-nestlings had about the same furcular fat score on day 25 (Fig. 1I,J), but the growth curves of the two groups had slightly different shapes (interaction agextreatment significant; Fig. 1I; Table 1). This may be partly due to the fact that placebo-nestlings by chance had more subcutaneous fat reserves on day 10 than future cort-nestlings and therefore fat was accumulated at a slightly lower rate until day 13 than in cort-nestlings.
Despite some significant variation in growth rate with sex, developmental stage and within-brood age differences, corticosterone treatment did not affect growth of the sexes and asynchronously hatched or less developed nestlings differentially in any of the measurements taken (Table 1).
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DISCUSSION |
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TOPSummaryINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONReferences |
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; Hull et al.,
2007) or restricting food over weeks in chicks (e.g.
Oyan and Anker-Nilssen, 1996;
Benowitz-Fredericks et al.,
2006). The plasma levels of corticosterone induced by the implants
were within the range occurring naturally in the smallest kestrel chicks
during nutritional stress (25–100 ng ml–1) and in
kestrel chicks after 20 min of handling (10–50 ng ml–1;
C.M., unpublished data).
Immediate effects of corticosterone on growth
During the period of elevated circulating corticosterone (days 13–16
of age), corticosterone treatment affected all growth parameters investigated,
but to very different degrees (reduction to 71% in feather growth rate, to 14%
in hand growth rate, to 26% in tarsus growth rate, to 0% in body mass increase
and no effect on subcutaneous fat stores). Feather growth was only reduced to
71%, although wing feather growth was at its maximum, and is a very costly and
inefficient process with only a 20% energetic efficiency of feather synthesis
in the kestrel (Dietz et al.,
1992). Feather growth reduction (to 84%) also extended into the
days when circulating corticosterone had returned to normal levels, as
observed in moulting starlings (Romero et
al., 2005). Growth of the skeletal elements of all extremities was
strongly reduced during the period of elevated corticosterone levels. Contrary
to feather growth, growth of the hand and tarsus recovered completely to the
(then low) rate of the control group directly after the period with elevated
corticosterone levels.
That body mass growth was completely stopped and body mass even reduced
under corticosterone treatment agrees with studies in precocial bird species,
such as chicken and quail (Davison et al.,
1983; Buyse et al.,
1987; Donker and Beuving,
1989; Siegel et al.,
1989; Bray, 1993;
Hayashi et al., 1994;
Post et al., 2003;
Dong et al., 2007;
Hull et al., 2007). Body mass
growth recovered after the treatment period. Because no birds were killed, we
cannot explore which parts of the body were most affected by corticosterone
treatment, except for growth of feathers and skeletal extremities (see above)
and fat stores. Corticosterone treatment did not reduce peripheral body fat
stores, demonstrating that nestlings were not in a normal fasting state, such
as under food restriction.
Corticosterone treatment thus had a differential effect on the growth of
different body parts and organs. This hierarchy in growth allocation under
elevated circulating corticosterone agrees partly with the hierarchy found in
food restriction experiments, indicating a regulating role of corticosterone
during food restriction. Structural growth is protected at the expense of more
flexible body tissues such as muscles
(Oyan and Anker-Nilssen, 1996;
Moe et al., 2004;
Benowitz-Fredericks et al.,
2006). Feather growth is even more strongly supported than bone
growth, similar to zebra finch nestlings raised with low-quality food
(Boag, 1987). An exception are
fat stores which are depleted first under food restriction, but kept under
corticosterone treatment; this may be due to the well-known fattening effect
of chronic corticosterone administration (e.g.
Davison et al., 1983;
Buyse et al., 1987). Flight
feathers are crucial for flight performance and were in their main growth
phase during elevated corticosterone levels; presumably, therefore, their
growth was most buffered. Additionally, hand and tarsus were in their final
growth phase during the treatment and had almost reached their definite
length. Thus corticosterone could only have a small effect on their final
size. Corticosterone treatment in another developmental stage may possibly
show a different growth allocation.
There may be two mechanisms by which corticosterone reduces feather growth.
The first is by interference with the growth hormone–IGF-1 axis
(Hochberg, 2002), the primary
control of postnatal growth (McNabb et
al., 1998). The suppressed growth rate of feathers (consisting of
up to 95% protein) can be explained by the inhibition of protein synthesis
with high corticosterone levels (Sapolsky
et al., 2000). The depressed feather growth rate in the days when
circulating corticosterone levels had returned to the level of the control
group could be the result of the continued presence of products induced by
corticosterone affecting gene transcription
(Sapolsky et al., 2000).
Glucocorticoids impair bone growth (1) indirectly with catabolic effects on
bone and cartilage protein, interfering with the growth hormone–IGF-1
axis and by disturbing normal calcium balance, and (2) directly, by impeding
anabolic processes at the growth plate and the adjacent tissues of the bones
(Hochberg, 2002). As a second
mechanism, corticosterone treatment may also have affected growth by reducing
appetite (Sapolsky et al.,
2000) and possibly by a reducing digestive efficiency or
increasing maintenance energy expenditure as observed in precocial chicks
(Dong et al., 2007). However,
the evidence of the effects of corticosterone on food intake is controversial.
Other studies observed increased or no change in food intake in quail and
chicken (Bray 1993,
Buyse et al., 1987;
Simon, 1984;
Davison et al., 1983) and
increased (Hayashi et al.,
1994) or decreased food conversion
(Siegel et al., 1989). Whether
kestrel nestlings could increase food intake by increased begging and
aggressiveness against siblings (Kitaysky
et al., 2003) remains to be shown. Food intake of cort-nestlings
during the 2 days after implantation was not measurably reduced compared with
placebo-nestlings (video observations of feeding rates, C.M., unpublished
data). This would indicate that elevated corticosterone increased energy
expenditure which contributed to the loss of body mass
(DuRant et al., 2008).
Compensatory growth
The compensatory growth pattern varied widely between body structures.
Accelerated growth occurred only in body mass and to a slight extent in
tarsus, while growth of hand and feather just resumed the growth rate of the
corresponding age (i.e. the growth rate of the placebo-nestlings). A prolonged
growth period probably occurred in body mass and feather length. Primary
feather length, measured at day 25, had only reached about 53% of its final
value; the primaries continue to grow after fledging. Therefore, we were
unable to assess whether the cort-nestlings prolonged or accelerated primary
growth after day 25 when their primary length was 10% shorter than in
placebo-nestlings. Growth of the two skeletal structures was terminated by day
25. Maturation of the tarsus and the hand bone seemed not to be slowed down,
which prevents prolonged or accelerated growth to reach a normal tarsus and
hand length.
Cort-nestlings did not accelerate body mass growth rate during the period
immediately following elevated corticosterone levels, but did so later before
fledging. On day 25, their body mass was only 9% lower than in
placebo-nestlings, compared with a body mass that was 14% lower on days 16 and
21, indicating a prolongation of the body mass growth phase. It is possible
that the cort-nestlings further compensated for their lag in body mass until
fledging by prolonging growth or by not reducing body mass just before
fledging, as normally developed placebo-nestlings do, similar to food-stressed
altricial song sparrows Melospiza melodia
(Searcy et al., 2004). As the
corticosterone-treated nestlings fledged about 2 days later than their placebo
siblings (C.M., unpublished data), it is likely that they prolonged the
build-up of body mass by 2 days and reached a similar fledging mass to their
placebo siblings.
To our knowledge, this is the first study that has examined the development
of body mass well after artificially elevated corticosterone levels returned
to normal. All other studies known to us stopped at the end of corticosterone
administration without monitoring potential compensatory growth. Studies
investigating a natural or experimental food restriction in altricial
nestlings, which lead to a similar lag in body mass to our corticosterone
treatment, found either a similar restoration of the growth rate to the normal
rates of the control group with prolonged growth
(Schew, 1995) or accelerated
growth (Negro et al., 1994;
Bize et al., 2006), so that the
reduction was at least partially compensated for. The timing and extent of the
compensatory growth seems to depend on the severity, the developmental phase
and the duration of the nutritional restriction.
Long-term effects of corticosterone on morphology and body condition
Only 2 days of elevated corticosterone levels resulted in a life-long
impact on morphology. Bone growth is completed before fledging and at this
point tarsus remained 4% shorter and hand skeleton 5% shorter than controls
[as in three altricial food-restricted species
(Boag, 1987;
Schew, 1995;
Searcy et al., 2004)], and
this was irreversible. The consequences of a shorter leg and wing length in
the kestrel are unknown. Concerning sexual selection, female kestrels select
males with shorter tarsi and do not discriminate short-winged males
(Hakkarainen et al., 1996), so
the slightly shorter cort-nestling males are probably not at a disadvantage.
However, this might be different in female kestrels, and in species without
reversed sexual size dimorphism, where smaller birds often have a reduced
fitness (Richner, 1989).
If wing feathers of cort-nestlings do not fully recover, wing length and
wing area would be somewhat smaller, possibly negatively affecting flight
performance and hunting capabilities and presumably survival. In male
kestrels, however, a smaller wing does not have to be a disadvantage.
Short-winged male kestrels are somewhat better hunters than longer-winged ones
(Hakkarainen et al., 1996). If
fledglings survive the first year, they have the opportunity to replace
shorter primaries with longer ones during moult the following summer. This
might be a good strategy, because accelerated feather growth is associated
with a lower feather quality (Dawson et
al., 2000) and general costs of compensatory growth
(Metcalfe and Monaghan,
2001).
Cort-nestlings fledged with similar fat stores to placebo nestlings.
However, if the reduction in body mass of cort-nestlings was not compensated
for until fledging, cort-nestlings would have fledged at a lower body mass.
Several studies have shown that body mass at fledging is a good predictor of
survival (Lindén et al.,
1992; Naef-Daenzer et al.,
2001). In kestrels, fledglings are still fed by their parents up
to 4 weeks after fledging and it is possible that the corticosterone-treated
nestlings could catch up then.
No differential effect of corticosterone on the sexes and ages
In all morphological parameters investigated corticosterone treatment did
not differentially affect the sexes and younger nestlings within the brood. We
did not find indications that later born, smaller nestlings are affected more
strongly than older, larger ones. Hence, we have no evidence that elevated
corticosterone levels amplify size-dependent mortality resulting from
asynchronous hatching. However, size differences between sexes and ages were
not large in our kestrels.
Conclusions
This study demonstrated in altricial and free-living nestlings that
elevated plasma levels of corticosterone alone, without food restriction,
suppress growth and, thus, that the action of corticosterone alone is involved
in the control of developmental plasticity. It follows that environmental
stressors without energetic restrictions (e.g. human disturbance, disease) may
have a growth-suppressing effect and consequently the potential to shape
phenotype. A relatively short disturbance of 2–3 days resulting in high
corticosterone levels can have far-reaching consequences on morphology and
fitness. In the context of conservation biology, it will be important to
investigate the effect of repeated high corticosterone levels, as may occur as
a response to repeated human disturbance, on growth and development.
With the corticosterone administered in this study, effective for only a few days, we provoked a reduced primary feather and tarsus length before fledging occurred, corresponding to that of siblings born 3 days later. However, feather, bone and body mass growth were reduced to different degrees. This indicates that corticosterone has not an overall suppressing effect on growth but a differential effect favouring presumably the most sensitive tissues of the actual developmental phase. Such a differential effect was also observed in nutritional restriction experiments. Because food shortage usually results in elevated corticosterone levels, this points to a steering role of corticosterone on growth allocation during nutritional restriction and other disturbances.
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Footnotes |
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References |
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TOPSummaryINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONReferences |
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Astheimer, L. B., Buttemer, W. A. and Wingfield, J. C. (1992). Interactions of corticosterone with feeding, activity and metabolism in passerine birds. Ornis Scand. 23,355 -365.[CrossRef]
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Eccleston, L. (2000). Rate of moult affects feather quality:
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