NDLI: Galanin regulates prolactin release and lactotroph proliferation

Content Provider	PubMed Central
Author	David, Wynick Small, Caroline J. Bacon, Andrea Holmes, Fiona E. Norman, Michael Ormandy, Christopher J. Kilic, Eser Kerr, Niall C. H. Ghatei, Md Talamantes, Frank Bloom, Stephen R. Pachnis, Vassilis
Copyright Year	1998
Abstract	The neuropeptide galanin is predominantly expressed by the lactotrophs (the prolactin secreting cell type) in the rodent anterior pituitary and in the median eminence and paraventricular nucleus of the hypothalamus. Prolactin and galanin colocalize in the same secretory granule, the expression of both proteins is extremely sensitive to the estrogen status of the animal. The administration of estradiol-17β induces pituitary hyperplasia followed by adenoma formation and causes a 3,000-fold increase in the galanin mRNA content of the lactotroph. To further study the role of galanin in prolactin release and lactotroph growth we now report the generation of mice carrying a loss-of-function mutation of the endogenous galanin gene. There is no evidence of embryonic lethality and the mutant mice grow normally. The specific endocrine abnormalities identified to date, relate to the expression of prolactin. Pituitary prolactin message levels and protein content of adult female mutant mice are reduced by 30–40% compared with wild-type controls. Mutant females fail to lactate and pups die of starvation/dehydration unless fostered onto wild-type mothers. Prolactin secretion in mutant females is markedly reduced at 7 days postpartum compared with wild-type controls with an associated failure in mammary gland maturation. There is an almost complete abrogation of the proliferative response of the lactotroph to high doses of estrogen, with a failure to up-regulate prolactin release, STAT5 expression or to increase pituitary cell number. These data further support the hypothesis that galanin acts as a paracrine regulator of prolactin expression and as a growth factor to the lactotroph.
Starting Page	12671
File Format	PDF
ISSN	10916490
e-ISSN	10916490
Journal	Proceedings of the National Academy of Sciences of the United States of America
Issue Number	21
Volume Number	95
Language	English
Publisher	The National Academy of Sciences
Publisher Date	1998-10-13
Access Restriction	Open
Rights Holder	The National Academy of Sciences
Subject Keyword	Research in Higher Education
Content Type	Text
Resource Type	Article
Subject	Multidisciplinary

Sl.	Authority	Responsibilities	Communication Details
1	Ministry of Education (GoI), Department of Higher Education	Sanctioning Authority	https://www.education.gov.in/ict-initiatives
2	Indian Institute of Technology Kharagpur	Host Institute of the Project: The host institute of the project is responsible for providing infrastructure support and hosting the project	https://www.iitkgp.ac.in
3	National Digital Library of India Office, Indian Institute of Technology Kharagpur	The administrative and infrastructural headquarters of the project	Dr. B. Sutradhar bsutra@ndl.gov.in
4	Project PI / Joint PI	Principal Investigator and Joint Principal Investigators of the project	Dr. B. Sutradhar bsutra@ndl.gov.in Prof. Saswat Chakrabarti will be added soon
5	Website/Portal (Helpdesk)	Queries regarding NDLI and its services	support@ndl.gov.in
6	Contents and Copyright Issues	Queries related to content curation and copyright issues	content@ndl.gov.in
7	National Digital Library of India Club (NDLI Club)	Queries related to NDLI Club formation, support, user awareness program, seminar/symposium, collaboration, social media, promotion, and outreach	clubsupport@ndl.gov.in
8	Digital Preservation Centre (DPC)	Assistance with digitizing and archiving copyright-free printed books	dpc@ndl.gov.in
9	IDR Setup or Support	Queries related to establishment and support of Institutional Digital Repository (IDR) and IDR workshops	idr@ndl.gov.in

Lack of prolactin receptor signaling in mice results in lactotroph proliferation and prolactinomas by dopamine-dependent and -independent mechanisms

Leukemia Inhibitory Factor Regulates Prolactin Secretion in Prolactinoma and Lactotroph Cells

Use of a prolactin-Cre/ROSA-YFP transgenic mouse provides no evidence for lactotroph transdifferentiation after weaning, or increase in lactotroph/somatotroph proportion in lactation

Oxytocin action at the lactotroph is required for prolactin surges in cervically stimulated ovariectomized rats

Epidermal growth factor receptor cross-talks with ligand-occupied estrogen receptor-α to modulate both lactotroph proliferation and prolactin gene expression

Impulse flow dependency of galanin release in vivo in the rat ventral hippocampus.

Wnt signaling in estrogen-induced lactotroph proliferation

Galanin regulates the postnatal survival of a subset of basal forebrain cholinergic neurons

Enhanced hippocampal noradrenaline and serotonin release in galanin-overexpressing mice after repeated forced swimming test

Galanin regulates prolactin release and lactotroph proliferation

Similar Documents

Lack of prolactin receptor signaling in mice results in lactotroph proliferation and prolactinomas by dopamine-dependent and -independent mechanisms

Leukemia Inhibitory Factor Regulates Prolactin Secretion in Prolactinoma and Lactotroph Cells

Use of a prolactin-Cre/ROSA-YFP transgenic mouse provides no evidence for lactotroph transdifferentiation after weaning, or increase in lactotroph/somatotroph proportion in lactation

Oxytocin action at the lactotroph is required for prolactin surges in cervically stimulated ovariectomized rats

Epidermal growth factor receptor cross-talks with ligand-occupied estrogen receptor-α to modulate both lactotroph proliferation and prolactin gene expression

Impulse flow dependency of galanin release in vivo in the rat ventral hippocampus.

Wnt signaling in estrogen-induced lactotroph proliferation

Galanin regulates the postnatal survival of a subset of basal forebrain cholinergic neurons

Enhanced hippocampal noradrenaline and serotonin release in galanin-overexpressing mice after repeated forced swimming test

Galanin regulates prolactin release and lactotroph proliferation