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

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 conductanc...

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Bibliographic Details
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
Description
Summary: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.

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