Somatostatin Receptors

Srikant, Coimbatore B.; Patel, Yogesh C.

doi:10.1007/978-1-4615-7886-4_16

Cited by 24 publications

(6 citation statements)

References 45 publications

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“…Interestingly, depression prevalence rates are not observed to be higher in girls prior to mid-puberty/ menarche [14][15][16][17][18][19][20], possibly reflecting ascertainment bias/reporting bias (depressed boys may be more likely to come to the attention of health care providers than depressed girls) or the possibility that prepubertal major depression is premonitory of bipolar illness [21] or that alterations in ovarian hormone levels proximate to menarche combine with earlier developmental risks in girls to increase vulnerability [22]. With some exceptions, the age of onset [4,5,[23][24][25][26] (but also see [27][28][29][30]), type of symptoms, severity, and likelihood of chronicity and recurrence [4,5,26,27,[31][32][33] (but also see [34][35][36][37][38][39][40]) display few consistent differences between men and women. Clinically, the following are more likely in women: present with anxiety, atypical symptoms, or somatic symptoms [7,26,27,37,39,41,42]; report symptoms, particularly in self-ratings [7,26,…”

Section: Overview Of Observed Sex Differences In Affective Disordersmentioning

confidence: 99%

Sex differences and the neurobiology of affective disorders

Rubinow

Schmidt²

2018

Neuropsychopharmacol

188

128

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Observations of the disproportionate incidence of depression in women compared with men have long preceded the recent explosion of interest in sex differences. Nonetheless, the source and implications of this epidemiologic sex difference remain unclear, as does the practical significance of the multitude of sex differences that have been reported in brain structure and function. In this article, we attempt to provide a framework for thinking about how sex and reproductive hormones (particularly estradiol as an example) might contribute to affective illness. After briefly reviewing some observed sex differences in depression, we discuss how sex might alter brain function through hormonal effects (both organizational (programmed) and activational (acute)), sex chromosome effects, and the interaction of sex with the environment. We next review sex differences in the brain at the structural, cellular, and network levels. We then focus on how sex and reproductive hormones regulate systems implicated in the pathophysiology of depression, including neuroplasticity, genetic and neural networks, the stress axis, and immune function. Finally, we suggest several models that might explain a sex-dependent differential regulation of affect and susceptibility to affective illness. As a disclaimer, the studies cited in this review are not intended to be comprehensive but rather serve as examples of the multitude of levels at which sex and reproductive hormones regulate brain structure and function. As such and despite our current ignorance regarding both the ontogeny of affective illness and the impact of sex on that ontogeny, sex differences may provide a lens through which we may better view the mechanisms underlying affective regulation and dysfunction.

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Section: Overview Of Observed Sex Differences In Affective Disordersmentioning

confidence: 99%

Sex differences and the neurobiology of affective disorders

Rubinow

Schmidt²

2018

Neuropsychopharmacol

188

128

View full text Add to dashboard Cite

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“…Moreover, in the latter study stimulatory effects on food intake were observed only in Fasted rats, and a significant inhibition of food intake was found during the first 60 min following central SS injection in previously sated rats (26). More recently it has been shown that icv administration of SS-14 or the SS analogue SMS 201-995 can prevent the anorexigenic effects of stressors such as restraint, although again the posterior pituitary and in other hypothalamic areas lying outside the blood-brain barrier, including the subfornical organ and the organum vasculosum of the lamina terminalis (14,15). Thus, it is possible that SS-28 may directly inhibit the release of plasma OT simply by diffusion to the magnocellular nerve terminals in the posterior pituitary, or by action on those anterior hypothalamic sites, including the forebrain circumventricular organs, which are known to play an essential role in the osmotic control of OT and AVP secretion (16,17).…”

Section: Discussionmentioning

confidence: 97%

Central Somatostatin Inhibits Cholecystokinin‐lnduced Oxytocin Secretion in Conscious Rats

Blackburn

Frederick

Strieker

et al. 1992

J Neuroendocrinology

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Recent studies have demonstrated the presence of fibres immunoreactive for somatostatin-28 (SS-28), which originate in the brainstem and selectively innervate the magnocellular oxytocin (OT) cells of the supraoptic nucleus. The potential physiological relevance of this pathway was investigated in the present study by measuring plasma OT levels in response to intraperitoneal administration of cholecystokinin in conscious male rats pretreated with intracerebroventricular injections of either SS-28 or artificial cerebrospinal fluid. Cholecystokinin treatment produced the expected marked rise in plasma OT levels in control rats pretreated intracerebroventricularly with artificial cerebrospinal fluid. However, this response was markedly blunted by prior intracerebroventricular administration of SS-28, even though SS-28 itself had no effect on basal plasma OT levels, nor did it impair OT release in response to hypertonic saline injection. These results demonstrate that centrally injected SS-28 can selectively block cholecystokinin-stimulated release of OT in rats, and support an inhibitory role for this peptide in brainstem-mediated neurohypophysial hormone secretion. Central SS-28 administration also elicited up to 3-fold increases in the amount of food ingested in 1 h by previously sated rats. These observations suggest the possibility that endogenous SS-28 may be involved in stimulating food intake in rats, and establish the basis for future studies to clarify the role of this neuropeptide in controlling ingestive behaviours.

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“…Although the non-specific binding of [^'I-Tyr1]-SRIF to the chicken pituitary membranes was high (approximately 50% of total binding), this was expected (Srikant & Patel, 19856) due to the accessibility of N-terminal residues to tissue peptidases (Presky & Schonbrunn, 1989). However, apart from the SRIF moieties, the specific binding of the tracer to the pituitary membranes was not competi¬ tively displaced by other hypothalamic releasing factors or brain peptides.…”

Section: Discussionmentioning

confidence: 97%

Somatostatin binding to chicken adenohypophysial membranes

Harvey

Attardo²,

Baidwan³

1990

Journal of Molecular Endocrinology

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[125I-Tyr1]-Somatostatin (SRIF)-binding sites were demonstrated on crude plasma membrane preparations from chicken pituitary glands. These binding sites were saturable and of high affinity (dissociation constant less than 1.0 nM) and low capacity (maximal binding capacity less than 200 fmol/mg protein) and were specific for SRIF moieties. The number and affinity of these binding sites in the caudal lobe of the pituitary, in which somatotrophs predominate, were similar to those in the cephalic lobe, in which lactotrophs and thyrotrophs are confined. Gonadotrophs are present in the caudal lobe, but whereas exogenous SRIF inhibited secretagogue-induced GH release from incubated pituitary glands, it had no effect on basal or secretagogue-induced LH release. The half-maximal binding of SRIF to the caudal lobe membranes (3 nM) was similar to that required for half-maximal suppression of TRH-induced GH release, suggesting a role for these binding sites in the regulation of GH secretion in birds.

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Somatostatin Receptors

Cited by 24 publications

References 45 publications

Sex differences and the neurobiology of affective disorders

Sex differences and the neurobiology of affective disorders

Central Somatostatin Inhibits Cholecystokinin‐lnduced Oxytocin Secretion in Conscious Rats

Somatostatin binding to chicken adenohypophysial membranes

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