Evidence for a luteinizing hormone surge center in the hypothalamus of the pig.
Studies were conducted to determine whether there is an LH surge generator in the hypothalamus of the pig. In experiment 1, 157-day-old ovariectomized (OVX) gilts received 1.5 microg estradiol benzoate (EB)/kg BW i.m. every 12 h from 0 through 24, 48, 72, or 96 h. Blood was sampled every 6 h from 3 to 36 h and every 3 h from 36 through 144 h. One of 3, 4 of 4, 4 of 4, and 2 of 3 gilts displayed an LH surge after treatment for 24, 48, 72, and 96 h, respectively. With the exception that time to maximum LH concentration was greater in gilts treated for 96 h than in those treated for 72 h (p < 0.05), parameters of the surge were similar among all gilts. In experiment 2a, an Alzet osmotic pump containing EB or vehicle was inserted s.c. behind an ear of 124-day-old OVX gilts, resulting in the following daily doses of EB: 0, 0.75, 1.50, or 3.00 microg/kg BW. Blood was sampled at 0, 2, 4, 6, and 8 h and every 8 h thereafter through 168 h to evaluate surge secretion of LH, and every 15 min for 8 h starting at 168 h to evaluate pulsatile LH secretion. Zero of 3, 0 of 2, 3 of 3, and 3 of 3 gilts displayed an LH surge after 0, 0.75, 1.50, and 3.00 microg EB/kg BW, respectively. Parameters of the surge were similar among gilts. Pulsatile LH secretion, evaluated 7 days after pump insertion, was significantly suppressed for estradiol-treated gilts compared to controls. In experiment 2b, at 182 days of age, 10 gilts used in experiment 2a plus 2 additional gilts in the original group prepared but not used for experiment 2a, were randomly assigned in groups (n=3) to the following daily doses of EB: 0, 0.19, 0.38, or 0.75 microg/kg BW, administered again by osmotic pump. Treatment and blood-sampling schedules were the same as in experiment 2a. Zero, 0, 1, and 2 gilts displayed an LH surge after treatment with 0, 0.19, 0.38, and 0.75 microg EB/kg BW, respectively. Parameters of the surge were similar among gilts that displayed an LH surge. Pulsatile LH secretion was significantly suppressed for estradiol-treated gilts compared to controls. Thus, the LH surge resulted from positive feedback stimulation of a specific surge generator rather than attenuation or dissipation of negative feedback inhibition of estradiol on a pulse generator.
Kraeling
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United States Department of Agriculture, R.B. Russell Agricultural Research Center, Athens, Georgia 30605, USA.
Johnson
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B
Barb
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Rampacek
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GB
D000818:Animals; D003864:Depression, Chemical; D004958:Estradiol / Q000008:administration & dosage / Q000031:analogs & derivatives* / Q000097:blood / Q000494:pharmacology; D005246:Feedback / Q000502:physiology; D005260:Female; D007030:Hypothalamo-Hypophyseal System / Q000187:drug effects / Q000502:physiology; D007031:Hypothalamus / Q000502:physiology*; D015918:Infusion Pumps, Implantable; D007273:Injections, Intramuscular; D007986:Luteinizing Hormone / Q000097:blood / Q000378:metabolism*; D010052:Ovariectomy; D013552:Swine
C074283:estradiol 3-benzoate; D004958:Estradiol; D007986:Luteinizing Hormone