Seasonal differences in the secretion of luteinising hormone and prolactin in response to N-methyl-DL-aspartate in starlings (Sturnus vulgaris).
In birds, unlike mammals, seasonal changes in reproductive function are associated with marked changes in the amount of gonadotrophin-releasing hormone (GnRH) stored in the hypothalamus. Prolonged exposure to long photoperiods leads to photorefractoriness after the breeding season. Photorefractory birds have low hypothalamic concentrations of chicken GnRH-I (cGnRH-I). Exposure to short photoperiods results in renewed cGnRH-I synthesis and increased hypothalamic stores. Birds are then photosensitive and subsequent exposure to an increase in photoperiod results in increased cGnRH-I secretion and gonadal maturation. However, it is unclear whether the reverse is true at the time of gonadal regression during long photoperiods (i.e. that a decrease in GnRH-I synthesis precedes regression). Hypothalamic stores of cGnRH-I, and possibly therefore of releasable GnRH-I, decrease after regression. Single injections of the glutamate agonist N-methyl-DL-aspartate (NMA) were used as a probe to assess releasable stores of cGnRH-I in male starlings at four physiologically different reproductive stages. Treatment induced the greatest increase in luteinising hormone (LH) in photosensitive birds in January, and a slight increase in sexually mature birds in April. There was a slight but significant increase in June, immediately after testicular regression, but no increase in fully photorefractory birds in September. These data confirm that photorefractoriness is associated with a lack of releasable cGnRH-I, but that decreased synthesis of cGnRH-I is not the proximate cause of regression. There was an increase in prolactin in response to NMA at all times. The magnitude of the response was proportional to pre-treatment concentrations, with the greatest response in June. It is suggested that high circulating prolactin may fine-tune the timing of gonadal regression in advance of the inhibition of cGnRH-I synthesis.
Dawson
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A
Centre for Ecology and Hydrology, Abbots Ripton, Huntingdon, Cambridgeshire, UK. asda@ceh.ac.uk
D000818:Animals; D018690:Excitatory Amino Acid Agonists / Q000494:pharmacology*; D007987:Gonadotropin-Releasing Hormone / Q000378:metabolism; D007031:Hypothalamus / Q000187:drug effects / Q000378:metabolism; D007986:Luteinizing Hormone / Q000097:blood / Q000378:metabolism*; D008297:Male; D016202:N-Methylaspartate / Q000494:pharmacology*; D011388:Prolactin / Q000097:blood / Q000378:metabolism*; D012621:Seasons; D012726:Sexual Behavior, Animal / Q000502:physiology; D046749:Starlings / Q000502:physiology*
D018690:Excitatory Amino Acid Agonists; D007987:Gonadotropin-Releasing Hormone; D016202:N-Methylaspartate; D011388:Prolactin; D007986:Luteinizing Hormone