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Growth hormone receptor in dopaminergic neurones regulates stress‐induced prolactin release in male mice
Author(s) -
Wasinski Frederick,
Chaves Fernanda M.,
Pedroso João A. B.,
Mansano Naira S.,
Camporez João Paulo,
Gusmão Daniela O.,
List Edward O.,
Kopchick John J.,
Frazão Renata,
Szawka Raphael E.,
Donato Jose
Publication year - 2021
Publication title -
journal of neuroendocrinology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.062
H-Index - 116
eISSN - 1365-2826
pISSN - 0953-8194
DOI - 10.1111/jne.12957
Subject(s) - endocrinology , medicine , dopaminergic , prolactin , biology , growth hormone receptor , median eminence , dopamine , tyrosine hydroxylase , hypothalamus , hormone , growth hormone
Arcuate nucleus (ARH) dopaminergic neurones regulate several biological functions, including prolactin secretion and metabolism. These cells are responsive to growth hormone (GH), although it is still unknown whether GH action on ARH dopaminergic neurones is required to regulate different physiological aspects. Mice carrying specific deletion of GH receptor (GHR) in tyrosine hydroxylase (TH)‐ or dopamine transporter (DAT)‐expressing cells were produced. We investigated possible changes in energy balance, glucose homeostasis, fertility, pup survival and restraint stress‐induced prolactin release. GHR deletion in DAT‐ or TH‐expressing cells did not cause changes in food intake, energy expenditure, ambulatory activity, nutrient oxidation, glucose tolerance, insulin sensitivity and counter‐regulatory response to hypoglycaemia in male and female mice. In addition, GHR deletion in dopaminergic cells caused no gross effects on reproduction and pup survival. However, restraint stress‐induced prolactin release was significantly impaired in DAT‐ and TH‐specific GHR knockout male mice, as well as in pegvisomant‐treated wild‐type males, whereas an intact response was observed in females. Patch clamp recordings were performed in ARH DAT neurones and, in contrast to prolactin, GH did not cause acute changes in the electrical activity of DAT neurones. Furthermore, TH phosphorylation at Ser 40 in ARH neurones and median eminence axonal terminals was not altered in DAT‐specific GHR knockout male mice during restraint stress. In conclusion, GH action in dopaminergic neurones is required for stress‐induced prolactin release in male mice, suggesting the existence of sex differences in the capacity of GHR signalling to affect prolactin secretion. The mechanism behind this regulation still needs to be identified.