Danny Rogers says:
?Stephen had to summarise a fairly complicated and messy branch of
endocrinology literature in his last message. I think he will agree that the
mechanism that kicks off moult is far from being a simple one ...?
I agree with Danny that the hormonal mechanisms that influence moulting in
birds are far from simple. I deliberately kept it simple for the purpose of
informing a general audience on Birding-aus about the physiology of
moulting. Nevertheless, the mechanisms are interesting, and will describe
them briefly below.
?...and that the precise role of thyroxines seems to vary a bit from
species to species -
e.g. in some thyroid activity is greatest in the weeks before moult, while
in others it is high during moult.?
Chris Corben also implies that you cannot produce a general model for moult
for birds because of interspecific differences. However, in general, the
roles of thyroid hormones do not vary between species. Rather, the
differences are in the timing of thyroxine (T4) secretions, bloodstream
levels of T4, the sensitivity of target organs to T4 action, and the
interaction of T4 and other hormones. These differences also depend very
much on the environmental conditions faced by the birds.
Of course, one occasionally comes across a species that hasn't "read the
rule book" and its physiology doesn't conform to the general model. But
this is rare.
There are two main hormones that are secreted by the bird?s thyroid gland,
triiodothyronine (T3) and thyroxine (T4). The functions of each of these
hormones and the factors which control there seceretion are well documented
(e.g. Assenmacher 1973, Astier 1980, Chandola et al. 1981, Hennemann 1986).
Thyroid hormone action is also pretty much the same in mammals and birds,
moulting in mammals pertaining to the shedding of hair rather than feathers!
The thyroid gland secretes T4 in greater concentrations than T3, but T3 is
much more potent than T4. In birds, concentrations of T4 can be twice as
high as T3, but the potency of T3 on target tissues can be as much as 6
times greater than that of T4. In addition, T4 can be converted to T3 in
peripheral regions of the body through a biochemical process called
deiodination.
Thyroid hormones have many functions in birds. These include regulation of
tissue and overall body growth, stimulation of carbohydrate metabolism,
regulation of moulting, elicitation of migratory urges and correct gonadal
(reproductive organ) development through interactions with testosterone.
Danny?s point about species variation in the timing of thyroid hormone
cycles and levels is a valid one. However, these factors are under the
influence of environmental factors and the physiological condition of the
bird, rather than interspecific differences.
Thyroid function increases within lengthening days, falls in ambient
temperature and an increased food (particularly carbohydrate intake). The
physiological interaction between the reproductive and thyroid hormones is
not fully understood. However, if thyroid activity is lowered during
breeding as a result of external factors (e.g. high ambient temperatures or
low carbohydrate intake), then the reproductive hormones appear to supress
that activity. Conversely, a lowering of reproductive hormone levels
towards the end of breeding contributes, in part, to the sudden increase in
thyroid activity, coinciding with increased food intake and other external
stimuli.
The interaction between the stimulatory and inhibitory effects should
explain the variation in the thyroid cycles alluded to by Danny. Birds that
have high thyroid hormone levels during the breeding period are probably
breeding under peak conditions ... plenty of food and other resources.
Reproductive hormones would be high under these conditions, but their
suppressive effects on thyroid activity are over-ridden by the external
stimuli.
Conversely, if breeding is resource (e.g. food) limited, such as in a poor
breeding season, then thyroid hormone activity is not stimulated, and
reproductive hormone levels would be low, but high enough, to keep that
activity suppressed.
Danny says:
?I'm just not convinced that the mechanism that kicks off a complete moult
is a
strait-jacket which will always force birds to perform a moult after an
opportunistic breeding attempt.?
Danny, I agree with this. The degree of moult (partial or complete) will
depend upon the levels of circulating thyroxines. If levels are high, then
a complete moult will occur; if they are low, then moulting may be partial
or not occur at all.
Optimal conditions for opportunistic breeding will stimulate intensive
breeding activity. Such activity, would result in a lot of wear and tear of
feathers, and it would be in the best interests of the bird to have them
replaced. Thyroid activity would be elevated only if adequate food and
other resources are still available at the conclusion of the breeding
attempt. If there is a sudden shortage of food (for instance) at the
conclusion of breeding, then not only would there be a decrease in the
secretion of T3 and T4 by the thyroid gland, but some of the secreted T4
(thyroxine: the moulting hormone) will be converted to T3 to help
metabolise carbohydrate stores in the body (i.e. body fat). This in turn,
would reduce the probability of a complete moult.
Therefore, to answer David James? points, moulting is NOT a liability to a
bird by being tied to breeding, it is a very GOOD adaptation. Intensive
breeding activity wears out feathers. Environmental conditions that
generally favour post-breeding moult in Australian passerines usually
follow conditions that favour good breeding conditions. The feathers are
not as worn if breeding is suppressed, this also usually means that
environmental conditions are not suitable for elevated thyroxine activity,
and so moulting is partial or does not occur.
Oh well, enough said. My apologies for dominating Birding-aus with a
discussion of bird physiology, but I hope a few of you have found it
interesting. I?ve said a few controversial things here. I?m sure they have
stirred a few people and will elicit further response!
Kind regards.
Stephen
References:
Assenmacher, I. (1973). The peripheral endocrine glands. In: Farner, D.S.,
King, J.R. & Parkes, K.C. (eds). Avian Biology, Vol. 3 (Academic Press, New
York).
Astier, H. (1980). Thyroid gland in birds: structure and function. In:
Epple, A. & Stetson, M.H. (eds). Avian Endocrinology (Academic Press, New
York).
Chandola, A., Pathak, V.K. & Bhatt, D. (1981). Seasonality in avian thyroid
function. In: Pethes, G., Peczely, P. & Rudas, P. (eds). Recent Advances of
Avian Endocrinology (Akademiai Kiado & Pergamon Press, Budapest).
Hennemann, G. (ed). Thyroid Hormone Metabolism (Marcel Dekker Inc., New York).
************************************************************
Dr Stephen Ambrose
Research Manager
Birds Australia (Royal Australasian Ornithologists Union)
Australian Bird Research Centre
415 Riversdale Road,
Hawthorn East,
VIC 3123.
Tel: +61 3 9882 2622
Fax: +61 3 9882 2677
Email:
1997 Australian Bird Research Directory is on Birds Australia's
home page: <http://www.vicnet.net.au/~birdsaus>.
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