Biochemical and Functional Properties of Somatostatin Receptors

  title={Biochemical and Functional Properties of Somatostatin Receptors},
  author={Stephanie Rens‐Domiano and Terry D. Reisine},
  journal={Journal of Neurochemistry},
The tetradecapeptide somatostatin (SRIF) exerts diverse biological actions in the endocrine and nervous systems (1, 2). It is the major physiological inhibitor of growth hormone secretion from the anterior pituitary and insulin and glucagon release from the pancreatic islets and also regulates gastric acid secretion from the gut (3–6). SRIF is also expressed in extrahypothalamic locations in the brain, where it has a role in controlling cognitive functions (7, 8). Furthermore, in the striatum… 

Molecular biology of somatostatin receptors.

The first evidence for somatostatin-like activity came from studies of Krulich et al. (17), who described a factor in hypothalamic extracts that inhibited GH secretion from anterior pituitaries in culture.

Somatostatin receptors in the central nervous system

Somatostatin receptors and disease : role of receptor subtypes

Along with this variety of actions of SST, somatostatin receptors (SSTR) have been detected in most of the target organs of the peptide and suggested that SST could have a role in the treatment of disease due to hyperfunction of these systems.

Multiple intracellular effectors modulate physiological functions of the cloned somatostatin receptors.

Clinical and post-mortem observations on Alzheimer's patients, as well as experimental studies in animal models, have suggested that this peptide may be an important regulator of cognitive functions and in support of this are the observations that the concentration of somatostatin in the brain is reduced in patients with Alzheimer’s dementia.

Somatostatin: physiology and clinical applications.

  • A. Shulkes
  • Medicine, Biology
    Bailliere's clinical endocrinology and metabolism
  • 1994

Ionic Mechanisms Governing the Control of Growth Hormone Secretion by Somatostatin

This chapter will be restricted to the mechanisms (primarily ionic) by which SS inhibits growth hormone (GH) release and the ionic mechanisms by which growth hormone releasing factor stimulates the acute release of GH via cyclic AMP (cAMP) and cytosolic free Ca++ ([Ca++]i) as second messengers.



Somatostatin mediation of adenohypophysial secretion.

This chapter will focus on hypothalamic somatostatin, its neural localization, regulation of secretion, physiological role in GH and TSH regulation, and mechanism of action on the anterior pituitary.

Purification of Somatostatin Receptors

Receptor binding of somatostatin-28 is tissue specific

It is suggested here that the greater potency of S-28 for inhibiting growth hormone secretion is because it binds to pituitary S-14 receptors with 3.2-fold higher affinity than does S- 14 in the central nervous system.

Selective effects of somatostatin-14, -25 and -28 on in vitro insulin and glucagon secretion

It is reported that SRif-28 and SRIF-25 are more potent thanSRIF-14 in the inhibition of insulin release, but that SR IF-14 preferentially inhibits glucagon release, indicating that their differential release may be physiologically important.

Functional somatostatin receptors on a rat pancreatic acinar cell line.

It is concluded that AR4-2J cells exhibit functional somatostatin receptors that retain both specificity and affinity of the pancreatic acinar cell somatstatin receptors and act via the pertussis toxin-sensitive guanine nucleotide-binding protein Ni to inhibit adenylate cyclase.

Differential expression of somatostatin receptor subtypes in brain

Several regions of the brain reported to contain dense somatostatin-like immunoreactive terminal fields and receptor binding sites were devoid of both SSTR1 and SSTR2 mRNA, suggesting the existence of additional SSTR subtypes.

Somatostatin in the central nervous system: Physiology and pathological modifications

  • J. Epelbaum
  • Biology, Medicine
    Progress in Neurobiology
  • 1986

Somatostatin inhibits vasoactive intestinal peptide-stimulated cyclic adenosine monophosphate accumulation in GH pituitary cells.

It is concluded that SRIF inhibits VIP-stimulated cAMP accumulation by a receptor-mediated process that may be causally related to the ability of SRIF to inhibit VIP-dependent PRL secretion.

Somatostatin-28: selective action on the pancreatic beta-cell and brain.

SS-28 compared to SS-14 shows pancreatic beta-cell and brain selectivity of action and D-Trp substitution in position 28 of SS-28 increase potency to 2600 times that ofSS-14 for inhibition of arginine induced insulin secretion.