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1 Department of Internal Medicine, University of Virginia, Charlottesville, VA, USA
2 Department of Internal Medicine, Mayo Clinic, Rochester, MN, USA
* To whom correspondence should be addressed. E-mail: veldhuis.johannes{at}mayo.edu.
Growth hormone (GH) pulsatility requires periventricular-nuclear somatostatin (SRIFPeV), arcuate-nuclear (ArC) GH-releasing hormone [GHRH] and systemic GH autofeedback. However, no current formalism interlinks these regulatory loci in a manner that generates self-renewable GH dynamics. The latter must include in the adult rat: (i) infrequent volleys of high-amplitude GH peaks in the male; (ii) frequent discrete low-amplitude GH pulses in the female; (iii) disruption of the male pattern by severing SRIFPeV outflow to ArC; (iv) stimulation of GHRH and GH secretion by CNS delivery of SRIF; (v) inhibition of GH release by central exposure to GHRH; and (vi) a rebound-like burst of GHRH secretion induced by stopping peripheral infusion of SRIF. The present study validates by computer-assisted simulations a simplified ensemble formulation that predicts each of the foregoing six outcomes, wherein: (a) blood-borne GH stimulates SRIFPeV secretion after a long time latency; (b) SRIFPeV inhibits both pituitary GH and ArC GHRH release; (c) ArC GHRH and SRIFArC oscillate reciprocally with brief time delay; and (d) SRIFPeV represses and disinhibits the putative GHRH-SRIFArC oscillator. According to the present analytical construction, time-delayed feedforward and feedback signaling among SRIFPeV, ArC GHRH and SRIFArC could endow the complex physiological patterns of GH secretion in the male and female.
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