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...
Guardado en:
| Autores principales: | , , , , , , , , , , |
|---|---|
| Formato: | SER |
| Materias: | |
| Acceso en línea: | http://hdl.handle.net/20.500.12110/paper_03013073_v38_n_p59_GarciaTornadu |
| Aporte de: |
| id |
todo:paper_03013073_v38_n_p59_GarciaTornadu |
|---|---|
| record_format |
dspace |
| spelling |
todo:paper_03013073_v38_n_p59_GarciaTornadu2023-10-03T15:18:20Z Neurotransmitter modulation of the GHRH-GH axis García-Tornadu, I. Risso, G. Perez-Millan, M.I. Noain, D. Diaz-Torga, G. Low, M.J. Rubinstein, M. Becu-Villalobos, D. Artz E. Bronstein Guitelman M. 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. SER info:eu-repo/semantics/openAccess http://creativecommons.org/licenses/by/2.5/ar 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 García-Tornadu, I. Risso, G. Perez-Millan, M.I. Noain, D. Diaz-Torga, G. Low, M.J. Rubinstein, M. Becu-Villalobos, D. Artz E. Bronstein Guitelman M. 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. |
| format |
SER |
| author |
García-Tornadu, I. Risso, G. Perez-Millan, M.I. Noain, D. Diaz-Torga, G. Low, M.J. Rubinstein, M. Becu-Villalobos, D. Artz E. Bronstein Guitelman M. |
| author_facet |
García-Tornadu, I. Risso, G. Perez-Millan, M.I. Noain, D. Diaz-Torga, G. Low, M.J. Rubinstein, M. Becu-Villalobos, D. Artz E. Bronstein Guitelman M. |
| author_sort |
García-Tornadu, I. |
| 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 |
| url |
http://hdl.handle.net/20.500.12110/paper_03013073_v38_n_p59_GarciaTornadu |
| work_keys_str_mv |
AT garciatornadui neurotransmittermodulationoftheghrhghaxis AT rissog neurotransmittermodulationoftheghrhghaxis AT perezmillanmi neurotransmittermodulationoftheghrhghaxis AT noaind neurotransmittermodulationoftheghrhghaxis AT diaztorgag neurotransmittermodulationoftheghrhghaxis AT lowmj neurotransmittermodulationoftheghrhghaxis AT rubinsteinm neurotransmittermodulationoftheghrhghaxis AT becuvillalobosd neurotransmittermodulationoftheghrhghaxis AT artze neurotransmittermodulationoftheghrhghaxis AT bronstein neurotransmittermodulationoftheghrhghaxis AT guitelmanm neurotransmittermodulationoftheghrhghaxis |
| _version_ |
1807315137042841600 |