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Titolo:
HYPOTHALAMIC AND HYPOPHYSEAL REGULATION OF GROWTH-HORMONE SECRETION
Autore:
BLUETPAJOT MT; EPELBAUM J; GOURDJI D; HAMMOND C; KORDON C;
Indirizzi:
INSERM,UNITE RECH DYNAM SYST NEUROENDOCRINIENS,U159,2TER RUE ALESIA F-75014 PARIS FRANCE
Titolo Testata:
Cellular and molecular neurobiology
fascicolo: 1, volume: 18, anno: 1998,
pagine: 101 - 123
SICI:
0272-4340(1998)18:1<101:HAHROG>2.0.ZU;2-N
Fonte:
ISI
Lingua:
ENG
Soggetto:
MESSENGER-RIBONUCLEIC-ACID; RAT ANTERIOR-PITUITARY; GH-RELEASING HORMONE; OBESE ZUCKER RATS; ADULT MALE-RAT; TRANSCRIPTION FACTOR GHF-1/PIT-1; STIMULATES SOMATOSTATIN RELEASE; NEUROPEPTIDE-Y CONCENTRATIONS; SIGNAL-TRANSDUCTION PATHWAYS; C-FOS GENE;
Keywords:
GROWTH HORMONE; GROWTH HORMONE RELEASING HORMONE; SOMATOSTATIN; NEUROPEPTIDES; THYROID HORMONES; STEROID HORMONES; CALCIUM; ACROMEGALY; DWARFISM; DIABETES; NEUROIMMUNE INTERACTIONS; PACEMAKER ACTIVITY;
Tipo documento:
Review
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Science Citation Index Expanded
Science Citation Index Expanded
Citazioni:
149
Recensione:
Indirizzi per estratti:
Citazione:
M.T. Bluetpajot et al., "HYPOTHALAMIC AND HYPOPHYSEAL REGULATION OF GROWTH-HORMONE SECRETION", Cellular and molecular neurobiology, 18(1), 1998, pp. 101-123

Abstract

1. Regulation of pulsatile secretion of growth hormone (GH) relies onhypothalamic neuronal loops, major transmitters involved in their operation are growth hormone releasing hormone (GHRH) synthetized mostly in arcuate nucleus (ARC) neurons, and somatostatin (SRIH), synthetizedboth in hypothalamus periventricular (PVe) and ARC neurons. 2. Neurons synthetizing both peptides can inhibit each other in a reciprocal manner. Other neuropeptides synthetized in ARC neurons, such as galanin,or in ARC interneurons, such as neuropeptide Y (NPY), are able to modulate synthesis and release of GHRH and SRIH into the hypothalamohypophyseal portal system. 3. In addition, the hitherto uncharacterized endogenous ligand of the recently cloned growth hormone releasing peptidereceptor, expressed mostly in the ARC, triggers GH release, presumably by actions on ARC interneurons. 4. Thyroid, gonadal, and adrenal steroid hormones also affect the GHRH-SRIH balance; a differential distribution of sex steroid receptors in the ARC and the PVe is likely to account for the different pattern of GH secretion in male and female animals. 5. Growth hormone itself is able to inhibit the amplitude of GH secretory episodes and to increase their frequency, by entering the brain (presumably by receptor-mediated internalization at the level of the choroid plexus) and acting subsequently on ARC neurons. 6. At the pituitary level, major neurotransmitters regulating GH cells act on receptors of the VIP/PACAP/GHRH family and of the somatostatin family, inparticular, sst2 and sst3. Those are coupled to accumulation of cAMP as a second messenger. 7. In addition, patch-clamp experiments and measurement of intracellular Ca2+ indicate that GH cells present characteristic, GHRH-dependent, but self-maintained Ca2+ spikes and [Ca2+](i) transients, which reflect adaptive mechanisms to constraints of episodic release. 8. Recent data on transcription factors affecting GH gene expression and somatotrope differentiation are also summarized. 9. Regulation and differentiation of somatotropes also depend upon paracrineprocesses within the pituitary itself and involve growth factors and several neuropeptides, for instance, vasoactive intestinal peptide, angiotensin 2, endothelin, and activin. 10. Finally, characteristic changes occur in the GH secretory pattern under discrete, pathological conditions, such as abnormal growth and dwarfism, diabetes, and acromegaly, as well as during inflammatory processes.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 30/03/20 alle ore 19:43:03