Neurotransmitter modulation of the GHRH-GH axis

The role of dopaminergic receptors in the control of GH release remains controversial. The dopamine receptor 2 (D2R) knockout mouse represents a useful model to study the participation of the D2R on growth and GHRH-GH regulation. These knockout mice have hyperprolactinemia and lactotrope hyperplasia...

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Publicado:	2010
Materias:	cyclic AMP dopamine 2 receptor growth hormone growth hormone releasing factor levodopa messenger RNA neurotransmitter prolactin somatostatin acromegaly dopamine release genotype growth hormone deficiency growth hormone release human hyperprolactinemia hypophysis cell hypothalamus knockout mouse nonhuman priority journal protein expression review Acromegaly Animals Dopamine Growth Growth Hormone Growth Hormone-Releasing Hormone Humans Mice Neurotransmitter Agents Receptors, Dopamine D2
Acceso en línea:	https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_03013073_v38_n_p59_GarciaTornadu http://hdl.handle.net/20.500.12110/paper_03013073_v38_n_p59_GarciaTornadu
Aporte de:	Biblioteca Digital - Facultad de Ciencias Exactas y Naturales (UBA) de Universidad de Buenos Aires

id	paper:paper_03013073_v38_n_p59_GarciaTornadu
record_format	dspace
spelling	paper:paper_03013073_v38_n_p59_GarciaTornadu2023-06-08T15:27:54Z Neurotransmitter modulation of the GHRH-GH axis cyclic AMP dopamine 2 receptor growth hormone growth hormone releasing factor levodopa messenger RNA neurotransmitter prolactin somatostatin acromegaly dopamine release genotype growth hormone deficiency growth hormone release human hyperprolactinemia hypophysis cell hypothalamus knockout mouse nonhuman priority journal protein expression review Acromegaly Animals Dopamine Growth Growth Hormone Growth Hormone-Releasing Hormone Humans Mice Neurotransmitter Agents Receptors, Dopamine D2 The role of dopaminergic receptors in the control of GH release remains controversial. The dopamine receptor 2 (D2R) knockout mouse represents a useful model to study the participation of the D2R on growth and GHRH-GH regulation. These knockout mice have hyperprolactinemia and lactotrope hyperplasia, but unexpectedly, they are also growth retarded. In D2R knockout mice there is a significant decrease in somatotrope population, which is paralleled by decreased GH content and output from pituitary cells. The sensitivity of GHRH-induced GH and cAMP release is similar between genotypes, even though the response amplitude is lower in knockouts. We point to an involvement of D2R signaling at the hypothalamic level as dopamine did not release GH acting at the pituitary level, and both somatostatin and GHRH mRNA expression are altered in knockout mice. The similarity of the pituitary defect in the D2R knockout mouse to that of GHRH deficient models suggests a probable mechanism. Loss of dopamine signaling via hypothalamic D2Rs at a critical age may causeinadequate GHRH secretion subsequently leading to inappropriate somatotrope lineage development. Furthermore, GH pulsatility, which depends on a regulated temporal balance between GHRH and somatostatin output might be compromised in D2R knockout mice, leading to lower IGF-I, and growth retardation. Copyright © 2010 S. Karger AG, Basel. 2010 https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_03013073_v38_n_p59_GarciaTornadu http://hdl.handle.net/20.500.12110/paper_03013073_v38_n_p59_GarciaTornadu
institution	Universidad de Buenos Aires
institution_str	I-28
repository_str	R-134
collection	Biblioteca Digital - Facultad de Ciencias Exactas y Naturales (UBA)
topic	cyclic AMP dopamine 2 receptor growth hormone growth hormone releasing factor levodopa messenger RNA neurotransmitter prolactin somatostatin acromegaly dopamine release genotype growth hormone deficiency growth hormone release human hyperprolactinemia hypophysis cell hypothalamus knockout mouse nonhuman priority journal protein expression review Acromegaly Animals Dopamine Growth Growth Hormone Growth Hormone-Releasing Hormone Humans Mice Neurotransmitter Agents Receptors, Dopamine D2
spellingShingle	cyclic AMP dopamine 2 receptor growth hormone growth hormone releasing factor levodopa messenger RNA neurotransmitter prolactin somatostatin acromegaly dopamine release genotype growth hormone deficiency growth hormone release human hyperprolactinemia hypophysis cell hypothalamus knockout mouse nonhuman priority journal protein expression review Acromegaly Animals Dopamine Growth Growth Hormone Growth Hormone-Releasing Hormone Humans Mice Neurotransmitter Agents Receptors, Dopamine D2 Neurotransmitter modulation of the GHRH-GH axis
topic_facet	cyclic AMP dopamine 2 receptor growth hormone growth hormone releasing factor levodopa messenger RNA neurotransmitter prolactin somatostatin acromegaly dopamine release genotype growth hormone deficiency growth hormone release human hyperprolactinemia hypophysis cell hypothalamus knockout mouse nonhuman priority journal protein expression review Acromegaly Animals Dopamine Growth Growth Hormone Growth Hormone-Releasing Hormone Humans Mice Neurotransmitter Agents Receptors, Dopamine D2
description	The role of dopaminergic receptors in the control of GH release remains controversial. The dopamine receptor 2 (D2R) knockout mouse represents a useful model to study the participation of the D2R on growth and GHRH-GH regulation. These knockout mice have hyperprolactinemia and lactotrope hyperplasia, but unexpectedly, they are also growth retarded. In D2R knockout mice there is a significant decrease in somatotrope population, which is paralleled by decreased GH content and output from pituitary cells. The sensitivity of GHRH-induced GH and cAMP release is similar between genotypes, even though the response amplitude is lower in knockouts. We point to an involvement of D2R signaling at the hypothalamic level as dopamine did not release GH acting at the pituitary level, and both somatostatin and GHRH mRNA expression are altered in knockout mice. The similarity of the pituitary defect in the D2R knockout mouse to that of GHRH deficient models suggests a probable mechanism. Loss of dopamine signaling via hypothalamic D2Rs at a critical age may causeinadequate GHRH secretion subsequently leading to inappropriate somatotrope lineage development. Furthermore, GH pulsatility, which depends on a regulated temporal balance between GHRH and somatostatin output might be compromised in D2R knockout mice, leading to lower IGF-I, and growth retardation. Copyright © 2010 S. Karger AG, Basel.
title	Neurotransmitter modulation of the GHRH-GH axis
title_short	Neurotransmitter modulation of the GHRH-GH axis
title_full	Neurotransmitter modulation of the GHRH-GH axis
title_fullStr	Neurotransmitter modulation of the GHRH-GH axis
title_full_unstemmed	Neurotransmitter modulation of the GHRH-GH axis
title_sort	neurotransmitter modulation of the ghrh-gh axis
publishDate	2010
url	https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_03013073_v38_n_p59_GarciaTornadu http://hdl.handle.net/20.500.12110/paper_03013073_v38_n_p59_GarciaTornadu
_version_	1768546629004034048

Neurotransmitter modulation of the GHRH-GH axis

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