During the last decade, the GH axis has become the compelling focus of remarkably active and broad-ranging basic and clinical research. Molecular and genetic models, the discovery of human GHRH and its receptor, the cloning of the GHRP receptor, and the clinical availability of recombinant GH and IGF-I have allowed surprisingly rapid advances in our knowledge of the neuroregulation of the GH-IGF-I axis in many pathophysiological contexts. The complexity of the GHRH/somatostatin-GH-IGF-I axis thus commends itself to more formalized modeling (154, 155), since the multivalent feedback-control activities are difficult to assimilate fully on an intuitive scale. Understanding the dynamic neuroendocrine mechanisms that direct the pulsatile secretion of this fundamental growth-promoting and metabolic hormone remains a critical goal, the realization of which is challenged by the exponentially accumulating matrix of experimental and clinical data in this arena. To the above end, we review here the pathophysiology of the GHRH somatostatin-GH-IGF-I feedback axis consisting of corresponding key neurotransmitters, neuromodulators, and metabolic effectors, and their cloned receptors and signaling pathways. We propose that this system is best viewed as a multivalent feedback network that is exquisitely sensitive to an array of neuroregulators and environmental stressors and genetic restraints. Feedback and feedforward mechanisms acting within the intact somatotropic axis mediate homeostatic control throughout the human lifetime and are disrupted in disease. Novel effectors of the GH axis, such as GHRPs, also offer promise as investigative probes and possible therapeutic agents. Further understanding of the mechanisms of GH neuroregulation will likely allow development of progressively more specific molecular and clinical tools for the diagnosis and treatment of various conditions in which GH secretion is regulated abnormally. Thus, we predict that unexpected and enriching insights in the domain of the neuroendocrine pathophysiology of the GH axis are likely be achieved in the succeeding decades of basic and clinical research.

Pathophysiology of the neuroregulation of growth hormone secretion in experimental animals and the human

Neurochemical regulation of sleep

The GABA uptake inhibitor tiagabine promotes slow wave sleep in normal elderly subjects.

Treatment with the CRH1-receptor-antagonist R121919 improves sleep-EEG in patients with depression.

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Steiger A (Max Planck Institute of Psychiatry, Munich, Germany). Sleep and endocrinology (Minisymposium). J Intern Med 2003; 254: 13–22.



A bidirectional interaction between sleep electroencephalogram and endocrine activity is well established in various species including humans. Various hormones (peptides and steroids) participate in sleep regulation. A keyrole was shown for the reciprocal interaction between sleep-promoting growth hormone-releasing hormone (GHRH) and sleep-impairing corticotropin-releasing hormone (CRH). Changes in the GHRH : CRH ratio result in changes of sleep-endocrine activity. It is thought that the change of this ratio in favour of CRH contributes to aberrances of sleep during ageing and depression (shallow sleep, blunted GH and elevated cortisol). Besides GHRH, ghrelin and galanin enhance slow wave sleep. Somatostatin is another sleep-impairing factor. Neuropeptide Y acts as a CRH antagonist and induces sleep onset. There are hints that CRH promotes rapid eye movement sleep (REMS). In animals prolactin enhances REMS. In humans vasocactive intestinal polypeptide (VIP) appears to play a role in the temporal organization of sleep as, after VIP, the non-REMS–REMS cycle decelerated. Cortisol appears to enhance REMS. Finally, gonadal hormones participate in sleep regulation. Oestrogen replacement therapy and CRH-1 receptor antagonism in depression are beneficial clinical applications of sleep-endocrine research.

https://onlinelibrary.wiley.com/doi/pdf/10.1046/j.1365-2796.2003.01175.x

Sleep and endocrinology

Reduced efficacy of growth hormone-releasing hormone in modulating sleep endocrine activity in the elderly.

Intracerebroventrikulare Applikation von VIP fuhrte zu einer signifikanten Steigerung von REM-Schlaf in Ratten [6, 9], Kaninchen [7] und Katzen [3]. VIP stimuliert daneben die Wachstumshormon-Sekretion bei der Ratte [2] sowie der Prolaktinsekretion sowohl bei der Ratte [4] als auch beim Menschen [5, 8]. Auserdem gibt es Hinweise, das VIP eine Rolle bei der Regulation des circadianen Rhythmus uber einen Einflus auf den Nucleus suprachiasmaticus ausubt [1]. Wir untersuchten den Effekt von stundlichen pulsatilen peripheren Applikationen zwischen 22.00 und 1.00 Uhr von 4 × 10 µg VIP (n = 7) und 4 × 50 µg VIP (n = 10) auf den Schlaf und auf die nachtliche endokrine Aktivitat bei mannlichen Kontrollpersonen (20–30 Jahre alt) gegenuber Placebo. Nach Applikation von 4 × 10 µg VIP sank die Prolaktinkonzentration signifikant (Area under the curve AUC: 4651 ± 542 ng/ml x min nach VIP vs. 6293 + 856 ng/ml x min nach Placebo, im Zeitraum von 22.00 bis 7.00 Uhr, p < 0,05), wohingegen das Schlaf-EEG keine Veranderungen aufwies. Nach Gabe von 4 × 50 µg VIP wurde ein signifikanter Anstieg von Prolaktin beobachtet (22.00 bis 3.00 Uhr: 3526 ± 325 ng /ml x min vs. 2766 ± 313 ng/ml x min, p < 0, 01). Nach 4 × 50 µg VIP war der Cortisolnadir signifikant vorverlagert (62 ± 27 min unter VIP vs. 146 ± 19 min unter Placebo, p < 0,01, Zeit nach „Licht aus“). Zwischen 0.20 und 4.40 Uhr fand sich in Folge davon eine signifikante Erhohung der Cortisolkonzentration (11965 ± 1939 ng/ml x min vs. 7747 ± 1136 ng/ml x min, p < 0, 05).

Vasoaktives Intestinales Peptid (VIP) verlangsamt Non-REM/REM-Zyklen und moduliert die nachtliche Hormonsekretion des Menschen

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Reduced efficacy of growth hormone-releasing hormone in modulating sleep endocrine activity in the elderly.

Vasoaktives Intestinales Peptid (VIP) verlangsamt Non-REM/REM-Zyklen und moduliert die nachtliche Hormonsekretion des Menschen