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Photoperiodic Regulation of Seasonal Breeding in Birds
Author(s) -
SHARP PETER J.
Publication year - 2005
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1196/annals.1327.024
Subject(s) - biology , pars tuberalis , medicine , endocrinology , hypothalamus , dio2 , seasonal breeder , photoperiodism , circadian clock , circadian rhythm , melatonin , median eminence , hormone , prolactin , deiodinase , pituitary gland , triiodothyronine , zoology , botany
A bstract : Day length‐dependent breeding in birds commonly occurs in spring and summer, but may occur after exposure to complex changes in day length, as for example in transequatorial migrants. More rarely, some photoperiodic birds breed when day lengths are decreasing or are short. The flexibility of avian photoperiodic breeding strategies may reflect modifications to a common reproductive photoperiodic neuroendocrine system. This involves an extraretinal photoreceptor and a biological clock, which generates a circadian rhythm of photoinducibility to measure photoperiodic time. The pineal gland is not essential for the reproductive photoperiodic response. The current model of the avian photoperiodic response has been modified to accommodate short day breeders, by incorporating a role for seasonal changes in prolactin secretion in the termination of breeding. Analysis of the sites of expression of clock genes suggests that the biological clock for reproductive photoperiodic time measurement is in the medial basal hypothalamus. Photoperiodic signal transduction may involve a clock‐dependent local conversion of thyroxine to triiodothyronine (T 3 ) in the medial basal hypothalamus mediated by increased expression of the gene encoding type 2 iodothyronine deiodinase. This photoinduced increase in T 3 may stimulate the release of gonadotrophin‐releasing hormone (GnRH) through thyroid hormone receptors in the median eminence. These may mediate retraction of glial cell end‐feet ensheathing GnRH nerve terminals abutting onto the hypophysial portal vasculature, allowing GnRH to be released to stimulate gonadotrophin secretion.