Reproductive failure associated with heat stress is a well-known phenomenon. The mechanism involved in this failure is not clearly understood. In order to test a possible direct effect of heat stress on ovarian function, 36 White Leghorn laying hens were housed in individual cages in 2 temperature- and light-controlled rooms (n = 18). At 31 wk of age, one group was exposed daily for 12 h to high temperature (42 +/- 3 degrees C), and the second group was maintained under thermoneutral conditions (24 to 26 degrees C) and served as control. Body temperature, feed intake, egg production, and egg weight were recorded daily; heparinized blood samples were drawn every 3 d for plasma hormonal level of luteinizing hormone, follicular stimulating hormone, progesterone, 17beta-estradiol, and testosterone. Six days after exposure half of the birds in each group were killed, and the ovary and oviduct were weighed and preovulatory follicles removed and extracted for mRNA of Cytochrome P 450 aromatase, 17-alpha hydroxylase. The same procedure was repeated 9 d later with the rest of the birds. Short and long heat exposure caused significant hyperthermia and reduction of egg production, egg weight, ovarian weight, and the number of large follicles. In addition, a significant reduction in plasma progesterone and testosterone was detected 2 d after exposing the birds to heat stress, and plasma 17beta-estradiol was significantly reduced 14 d after initiation of heat stress. Short exposure to heat stress caused significant reduction in mRNA expression of cytochrome P450 17-alpha hydroxylase, exposing the birds to long-term heat stress caused significant reduction in expression of mRNA of both steroidogenic enzymes. No significant change was found in plasma luteinizing hormone and follicular stimulating hormone levels during the entire experimental period. We suggest a possible direct effect of heat stress on ovarian function.

Gonadotrophin-inhibitory hormone (GnIH), a hypothalamic RFamide, has been found to inhibit gonadotrophin secretion from the anterior pituitary gland originally in birds and, subsequently, in mammalian species. The gene encoding a transmembrane receptor for GnIH (GnIHR) was recently identified in the brain, pituitary gland and gonads of song bird, chicken and Japanese quail. The objectives of the present study are to characterise the expression of GnIHR mRNA and protein in the chicken pituitary gland, and to determine whether sexual maturation and gonadal steroids influence pituitary GnIHR mRNA abundance. GnIHR mRNA quantity was found to be significantly higher in diencephalon compared to either anterior pituitary gland or ovaries. GnIHR mRNA quantity was significantly higher in the pituitaries of sexually immature chickens relative to sexually mature chickens. Oestradiol or a combination of oestradiol and progesterone treatment caused a significant decrease in pituitary GnIHR mRNA quantity relative to vehicle controls. GnIHR-immunoreactive (ir) cells were identified in the chicken pituitary gland cephalic and caudal lobes. Furthermore, GnIHR-ir cells were found to be colocalised with luteinising hormone (LH)beta mRNA-, or follicle-stimulating hormone (FSH)beta mRNA-containing cells. GnIH treatment significantly decreased LH release from anterior pituitary gland slices collected from sexually immature, but not from sexually mature chickens. Taken together, GnIHR gene expression is possibly down regulated in response to a surge in circulating oestradiol and progesterone levels as the chicken undergoes sexual maturation to allow gonadotrophin secretion. Furthermore, GnIHR protein expressed in FSHbeta or LHbeta mRNA-containing cells is likely to mediate the inhibitory effect of GnIH on LH and FSH secretion.

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The effects of broiler breeder BW and nutrient intake on ovary morphology and plasma reproductive hormone profiles were examined at photostimulation (PS) (21 wk) and at sexual maturity (SM) in standard (STD) and low (LOW), or high (HIGH) BW birds provided either restricted (RF) or ad libitum (AL) access to feed between PS and SM. At PS, 30 Shaver Starbro pullets at target BW were assigned to the STD treatment, and birds either 20% heavier (HIGH) or lighter (LOW) assigned accordingly. Ten birds of each size group were processed immediately for carcass analysis and 10 birds assigned to each size by feed interaction group. Blood samples were taken at 3-d intervals beginning at PS and profiles constructed for estradiol-17beta, luteinizing hormone (LH), and follicle-stimulating hormone (FSH) to examine the relationship between body size, feeding level, and reproduction. Birds were processed for assessment of reproductive traits following SM. The AL birds reached SM with 11.0 large yellow follicles (LYF) (> 10 mm diameter) compared to 7.1 in RF birds. Small follicle atresia (< 5 mm diameter) was low in AL birds (10.3) compared to RF birds (32.3). The extent of small follicle atresia in RF birds was found to be inversely proportional to LYF number by stepwise regression. Increased small follicle atresia was associated with a longer sexual maturation period in RF birds (r = 0.619; P = 0.0003). Plasma estradiol-17beta concentration was greater in HIGH than in STD or LOW birds at PS, suggesting more advanced ovary development in HIGH birds. Estradiol-17beta profiles were similar in shape in all treatments, with the primary difference being the length of time prior to a substantial estradiol-17beta increase. Following PS, plasma LH and FSH concentrations of AL birds increased to levels nearly double that of RF birds, indicating a role for nutrient intake with rate of reproductive development. Plasma LH and FSH concentrations remained elevated for a greater time period in RF birds, however, possibly relating to the development of processes limiting LYF recruitment. This experiment demonstrated a modulation of reproductive hormone concentrations during sexual maturation by feeding level in conjunction with a sensitivity of the ovary to nutritional effects.

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