Abstract
GHRH and somatostatin are the important final common hypothalamic pathways in the control of somatotroph function and they act together in a concerted fashion to mediate this effect. Data accrued largely from in vivo studies suggest that many of the factors which modulate GH secretion do so through control or the somatostatinergic neurones in the hypothalamus against the background of an important priming action of GHRH. Acute inhibitory feedback control can occur through GH itself whereas chronic feedback control may well operate through IGF-I. There is no evidence that down-regulation or desensitisation of the somatotroph is an important in vivo event and variability in GH responsiveness to exogenously administered GHRH can be explained via a GH-mediated feedback pathway. The idea has emerged of a “hypothalamic cholinergic-somatostatinergic unit” by means of which acetyl choline tonically inhibits somatostatin release. This unit is sensitive to peripheral signals such as those mediated by glucose and GH itself. Further studies should now be directed towards understanding the nature of these modulatory interactions at the cellular level.
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