Effects of steroid hormones on the expression of Ca2+ activated K+ channels in in vitro pituitary cells of Atlantic cod (Gadus morhua)

• Main Author: Sætersmoen, Michelle Lu
• Format: Master Thesis
• Language: English
• Published: 2014
• Subjects: Ca2; activated; K; channels; BPG; axis; Atlantic; cod; steroid; hormones; atlantic cod; Gadus morhua
• Online Access: http://hdl.handle.net/10852/41723; http://urn.nb.no/URN:NBN:no-46176

The objective of the present study was to investigate the in vitro effects of the sex steroids testosterone (T), dihydrotestosterone (DHT), estradiol-17β (E2), or cortisol treatment on mRNA expression levels of Ca2+-activated K+ channel genes in Atlantic cod dispersed pituitary cells: big conductance (BK; kcnma2) intermediate conductance (SK4;kcnn4) and small conductance (SK1-3; kcnn1, kcnn2, kcnn3) channels. The exact way gonadotropins are regulated is not known but one hypothesis is that the regulation of gonadotrope cells that secreting Fsh and Lh can be regulated by the membrane expression of KCa which effects the way in which the cells respond to steroid hormones and other regulatory signals. Steroid hormone treatments were applied to Atlantic cod pituitary primary cell cultures at a concentration of 10-7M. Steroid hormones can exert a negative or positive feedback on the brain-pituitary-gonadal (BPG) axis which is a key component regulating the onset of puberty and sexual maturation in vertebrates. Fsh and Lh are gonadotropins that are essential in the BPG axis and are differentially regulated. In teleosts, these gonadotropins are synthesized and released by two different cells in the pituitary. No statistically significant effects of steroid hormones on mRNA expression of kcnn1 (SK1), kcnn1a (SK1a), kcnn2 (SK2), and kcnma2 (BK) were observed. Expression of kcnn3 (SK3) was significantly reduced after F treatment and the expression of kcnn4 (SK4) was also significantly reduced after T treatment and showed an inhibitory trend after DHT treatment. The effects of steroid hormones on sexual maturation are perhaps regulated partly via KCa channels, although more studies must be performed to prove this hypothesis.