| Budget Amount *help |
¥2,100,000 (Direct Cost: ¥2,100,000)
Fiscal Year 1987: ¥500,000 (Direct Cost: ¥500,000)
Fiscal Year 1986: ¥1,600,000 (Direct Cost: ¥1,600,000)
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| Research Abstract |
A series of experiments was carried out to analyse the mechanisms by which heat stress suppresses oestrous behaviour and causes anoestrus in farm animals. In experiment 1, normally cycling goats were subjected to a three temperature treatments, 25゜C(control), 35゜C(mild hot) and 40゜C(severe hot), and their behavioural and hormonal responses were examined. Plasma concentrations of oestradiol during the follicular phase decreased as the temperature increased, whereas there were no significant variations in the plasma LH levels among the treatments. The decrease of oestradiol was much more pronounced under severe-stress conditions, resulting in a delay in the onset of oestrus or anoestrus. In experiment 2, ovariectomized animals were challenged to exgeneous oestradiol infusion which simulated the preovulatory levels of plasma oestradiol in intact animals. Neither the time of the infusion nor the amount of oestradiol infused to elicit normal oestrous behaviour was different under control an
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d sever-stress conditions, whereas the doses of oestradiol required to trigger the LH surge were significantly larger in heat stressed animals. In experiment 3, one of the groups of severe-hot was treated with bromocriptine in order to assess a possible involvement of the heat stress-induced hyperprolactinaemia in the reduction of the ovarian activity and/or the sensitivity of the hypothalamo-pituitary axis. The bromocriptine treatment completely suppressed prolaction in heat stressed animals. While the treatment failed to improve ovarian oestradiol secretion, the delay of LH surge in heat stressed animals was restored to a normal range. Based on these results, it was concluded that 1) the direct cause of anoestrus under heat stress condition might be the reduction of the ovarian oestradiol secretion, 2) the responsiveness of the hypothalamo-pituitary axis to the positive feedback effect of oestradiol was also desensitized due to heat stress-induced hyperprolactinamia, and 3) the hyperprolactinaemia, however, would not be a major cause of the reduction of ovarian oestradiol secretion. Less
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