Prolactin receptor concentrations in the skin of mink during the winter fur growth cycle

✍ Scribed by Rose, Jack ;Garwood, Todd ;Jaber, Basem

• Publisher: John Wiley and Sons
• Year: 1995
• Tongue: English
• Weight: 570 KB
• Volume: 271
• Category: Article
• ISSN: 0022-104X
• DOI: 10.1002/jez.1402710307

✦ Synopsis

Abstract

The objectives of this study were to determine: 1) if the skin of mink might be a target organ for prolactin (PRL) by establishing if PRL binding sites (receptors) exist in the cell membranes of skin, and 2) if PRL receptor concentrations change during onset and progression of the winter fur growth cycle. Skin was collected on October 6, 1992 for characterization of PRL receptors and from July through December 1992 (N = 3 mink/month) to evaluate possible changes in PRL receptor concentrations during the fur growth cycle. PRL receptors were quantified using^125^I‐ oPRL in a validated radioreceptor assay. Scatchard analysis of saturation data revealed a single class of high‐affinity (K~d~=5.21 × 10^−11^±. 84M), low capacity (B~max~= 27.03 ± 3.37 fmoles/mg) binding sites. Only oPRL (40% displacement) and to a lesser extent oGH (3% displacement) inhibited the binding of^125^I‐oPRL to mink skin cell membranes. No inhibition of^125^I‐oPRL binding to membranes occurred in the presence of a 500‐fold excess of bTSH of oLH, indicating that the receptors were hormone specific. Concentrations of^125^I‐oPRL receptors during the onset and development of winter fur growth (July through November) exhibited no significant change. However, following completion of the winter fur growth cycle (December 1) PRL receptor concentration was significantly higher than all preceding months. The greater binding observed at that time may reflect a change in tissue sensitivity, in preparation for growth of the summer pelage. These data suggest to us that the skin of mink is a target organ for PRL and are consistent with the hypothesis that part of the affects of PRL on fur growth occur directly at the level of the skin. © 1995 Wiley‐Liss, Inc.