AJP - Endocrinology and Metabolism, Vol 271, Issue 1 E24-E30, Copyright © 1996 by American Physiological Society
Galanin gene expression in radiothyroidectomy-induced thyrotroph adenomas
J. F. Hyde, J. P. Moore Jr, K. W. Drake and D. G. Morrison
Department of Anatomy and Neurobiology, University of Kentucky College of Medicine, Lexington 40536, USA. jfhyde00@ukcc.uky.edu
Galanin gene expression is markedly increased in the anterior pituitary
glands of estrogen-treated rats (lactotroph hyperplasia) as well as human
growth hormone-releasing hormone transgenic mice (somatotroph hyperplasia).
The objective of this study was to examine galanin in a mouse model of
thyrotroph adenoma formation. Male mice were radiothyroidectomized by use
of iodine-131 (131I), and galanin peptide levels were assessed in the
hypothalamic-pituitary axis. Immunoreactive galanin concentrations in the
anterior pituitaries of 131I-treated mice were decreased 80% at 3, 6, 9,
and 12 mo after radiothyroidectomy. Galanin peptide levels in the
hypothalamus were decreased 20-25% at these times. Treatment with either
estradiol or 3,3',5-triiodo-L-thyronine increased galanin peptide
concentrations in the anterior pituitaries of 131I-treated mice, but
neither treatment restored galanin concentrations. Galanin mRNA levels were
decreased > 80% 1 yr after radiothyroidectomy. We conclude that, unlike
animal models of lactotroph and somatotroph hyperplasia, galanin gene
expression is suppressed throughout the development of thyrotroph adenomas,
suggesting that galanin does not have a stimulatory role in the
proliferation of thyrotrophs. Moreover, these data show that thyroid
hormones are important positive regulators of galanin gene expression in
the mouse and that estrogen may stimulate galanin gene expression in the
absence of thyroid hormones.
