Seasonal Differences in the Secretion of Luteinising Hormone and Prolactin in Response to N‐Methyl‐dl‐Aspartate in Starlings (Sturnus vulgaris)

Abstract

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.