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- Author: H. K. ELLIS x
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Search for other papers by W. B. WATKINS in
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Search for other papers by H. K. ELLIS in
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SUMMARY
[35S]Cysteine was injected intracisternally into guinea-pigs and 5 h later the soluble proteins of the neural lobe were subjected to electrophoresis on starch and polyacrylamide. In both systems approximately 80% of the total radioactivity was recovered in a single peak with an electrophoretic mobility corresponding to the position of the major protein component. The proteins present in the guinea-pig neural lobe were extracted in 0·1 m-HCl. Fractionation of the protein—neurohypophysial hormone complex on Sephadex G-75 resulted in the isolation of a protein which cross-reacted immunologically with an antiserum raised against porcine neurophysin II. The protein designated a neurophysin contained one molecule of lysine, isoleucine and tyrosine per molecule of protein. It contained no histidine or methionine and its minimum molecular weight was estimated as 8436 by amino acid analysis.
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Search for other papers by J. J. EVANS in
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SUMMARY
Pituitary glands were collected from a selection of 22 domestic and exotic mammalian species. The soluble proteins extracted from the neurohypophyses were characterized by horizontal starch-gel electrophoresis at pH 8·1. Those species which were closely related phylogenetically, e.g. fallow deer and muntjac deer, pig and hippopotamus, dog and coatimundi, and members of the primates, had similar and in some cases identical protein profiles. The ability of proteins extracted from the starch-gel to cross-react immunologically with an antiserum raised against porcine neurophysin-II was determined by microimmunodiffusion. Using this technique for the identification of neurophysins in conjunction with osmotic stimulation experiments, it was found that the number of major neurophysins present in the mammalian neurohypophyses studied varied from one in the guinea-pig and hedgehog to four in man. The concept of multiple neurophysins is discussed.
Search for other papers by H. F. Urbanski in
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Search for other papers by D. H. Ellis in
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Search for other papers by B. K. Follett in
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Golden hamsters were castrated and either maintained under short days of 9 h light and 15 h darkness (9L: 15D) or transferred to 12L: 12D, 13L: 11D or 16L:8D. Plasma concentrations of FSH and LH remained low under 9L: 15D and 12L: 12D for 6–8 weeks but rose markedly within 4 weeks under 13L: 11D and 16L: 8D, suggesting a more abrupt transition between non-stimulatory and maximally stimulatory photoperiods than found in Japanese quail.
Intact and castrated hamsters were exposed to natural photoperiods at a latitude of 51° 27' N (Bristol) for 12 months. In the intact animals plasma FSH and LH levels and the size of the testes decreased as the daylength shortened from 12·5 to 10·5 h during autumn. This was followed by a rise in FSH output in mid-winter with an upward trend in LH secretion. The ensuing testicular recrudescence was complete before the spring equinox. The results emphasize that under natural conditions the primary factor regulating gonadal growth is the development of refractoriness to short days. In castrated hamsters there was no significant seasonal trend in LH output. Levels of FSH remained unchanged until a peak occurred in January, the same time that a peak was seen in intact animals before testicular recrudescence. A similar peak occurred in castrated hamsters maintained in 9L: 15D in the laboratory. This suggests that even in the absence of gonadal steroid negative feedback. hypothalamo-pituitary activity changes during the photorefractory period.
Search for other papers by Karin L Gustafsson in
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Search for other papers by Sofia Movérare-Skrtic in
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Search for other papers by Helen H Farman in
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Department of Rheumatology and Inflammation Research, Institute of Medicine, Sahlgrenska Academy at University of Gothenburg, Gothenburg, Sweden
Search for other papers by Cecilia Engdahl in
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Search for other papers by Petra Henning in
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Search for other papers by Karin H Nilsson in
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Department of Rheumatology and Inflammation Research, Institute of Medicine, Sahlgrenska Academy at University of Gothenburg, Gothenburg, Sweden
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Department of Rheumatology and Inflammation Research, Institute of Medicine, Sahlgrenska Academy at University of Gothenburg, Gothenburg, Sweden
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Department of Rheumatology and Inflammation Research, Institute of Medicine, Sahlgrenska Academy at University of Gothenburg, Gothenburg, Sweden
Search for other papers by Ulrika Islander in
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Department of Veterans Affairs Medical Center, Long Beach, Long Beach, California, USA
Search for other papers by Ellis Levin in
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Department of Drug Treatment, Sahlgrenska University Hospital, Region Västra Götaland, Gothenburg, Sweden
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Search for other papers by Marie K Lagerquist in
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Selective estrogen receptor modulators (SERMs) act as estrogen receptor (ER) agonists or antagonists in a tissue-specific manner. ERs exert effects via nuclear actions but can also utilize membrane-initiated signaling pathways. To determine if membrane-initiated ERα (mERα) signaling affects SERM action in a tissue-specific manner, C451A mice, lacking mERα signaling due to a mutation at palmitoylation site C451, were treated with Lasofoxifene (Las), Bazedoxifene (Bza), or estradiol (E2), and various tissues were evaluated. Las and Bza treatment increased uterine weight to a similar extent in C451A and control mice, demonstrating mERα-independent uterine SERM effects, while the E2 effect on the uterus was predominantly mERα-dependent. Las and Bza treatment increased both trabecular and cortical bone mass in controls to a similar degree as E2, while both SERM and E2 treatment effects were absent in C451A mice. This demonstrates that SERM effects, similar to E2 effects, in the skeleton are mERα-dependent. Both Las and E2 treatment decreased thymus weight in controls, while neither treatment affected the thymus in C451A mice, demonstrating mERα-dependent SERM and E2 effects in this tissue. Interestingly, both SERM and E2 treatments decreased the total body fat percent in C451A mice, demonstrating the ability of these treatments to affect fat tissue in the absence of functional mERα signaling. In conclusion, mERα signaling can modulate SERM responses in a tissue-specific manner. This novel knowledge increases the understanding of the mechanisms behind SERM effects and may thereby facilitate the development of new improved SERMs.
