Somatostatinergic systems in brain: Networks and functions

Viollet, Cécile; Lepousez, Gabriel; Loudes, Catherine; Videau, Catherine; Simon, A.; Epelbaum, Jacques

doi:10.1016/j.mce.2007.09.007

Cited by 179 publications

(206 citation statements)

References 115 publications

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“…In mammals, i.c.v. administration of SS1 increases locomotor activity through the activation of SSTR2 and SSTR4, whereas its depletion has been reported to induce learning and memory deficits, mediated by SSTR2 (Viollet et al 2008).…”

Section: Uts2r5mentioning

confidence: 97%

“…It inhibits glutamate release presynaptically by acting through SSTR1, SSTR2, or SSTR5, depending on the anatomical structure, thus leading to the activation of potassium leak current and inhibition of voltagedependent calcium currents. SS1 also exhibits long-lasting effects on glutamatergic synapses by modulating long-term potentiation (Viollet et al 2008). In mammals, i.c.v.…”

Section: Uts2r5mentioning

confidence: 99%

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MOLECULAR EVOLUTION OF GPCRS: Somatostatin/urotensin II receptors

Tostivint¹,

Daza²,

Bergqvist³

et al. 2014

Journal of Molecular Endocrinology

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Somatostatin (SS) and urotensin II (UII) are members of two families of structurally related neuropeptides present in all vertebrates. They exert a large array of biological activities that are mediated by two families of G-protein-coupled receptors called SSTR and UTS2R respectively. It is proposed that the two families of peptides as well as those of their receptors probably derive from a single ancestral ligand-receptor pair. This pair had already been duplicated before the emergence of vertebrates to generate one SS peptide with two receptors and one UII peptide with one receptor. Thereafter, each family expanded in the three whole-genome duplications (1R, 2R, and 3R) that occurred during the evolution of vertebrates, whereupon some local duplications and gene losses occurred. Following the 2R event, the vertebrate ancestor is deduced to have possessed three SS (SS1, SS2, and SS5) and six SSTR (SSTR1-6) genes, on the one hand, and four UII (UII, URP, URP1, and URP2) and five UTS2R (UTS2R1-5) genes, on the other hand. In the teleost lineage, all these have been preserved with the exception of SSTR4. Moreover, several additional genes have been gained through the 3R event, such as SS4 and a second copy of the UII, SSTR2, SSTR3, and SSTR5 genes, and through local duplications, such as SS3. In mammals, all the genes of the SSTR family have been preserved, with the exception of SSTR6. In contrast, for the other families, extensive gene losses occurred, as only the SS1, SS2, UII, and URP genes and one UTS2R gene are still present.

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Section: Uts2r5mentioning

confidence: 97%

Section: Uts2r5mentioning

confidence: 99%

MOLECULAR EVOLUTION OF GPCRS: Somatostatin/urotensin II receptors

Tostivint¹,

Daza²,

Bergqvist³

et al. 2014

Journal of Molecular Endocrinology

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“…Peptides from this precursor are involved in physiological mechanisms like nausea and anxiety (35,36). Somatostatin, also called somatotropin-release inhibiting factor, is a multifunctional hormone involved in the inhibition of the release of other hormones and the exocrine secretions (37). A peptide RLELQR2SANSNPAMAPRE2RK derived from this precursor was up-regulated of 73% (p ϭ 0.007) by nicotine.…”

Section: Table I Changed Prohormone-derived Peptides and Unchanged Knmentioning

confidence: 99%

Chronic Nicotine Treatment Impacts the Regulation of Opioid and Non-opioid Peptides in the Rat Dorsal Striatum

Petruzziello

Falasca

Andrén

et al. 2013

Molecular & Cellular Proteomics

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The chronic use of nicotine, the main psychoactive ingredient of tobacco smoking, alters diverse physiological processes and consequently generates physical dependence. To understand the impact of chronic nicotine on neuropeptides, which are potential molecules associated with dependence, we conducted qualitative and quantitative neuropeptidomics on the rat dorsal striatum, an important brain region implicated in the preoccupation/ craving phase of drug dependence. We used extensive LC-FT-MS/MS analyses for neuropeptide identification and LC-FT-MS in conjunction with stable isotope addition for relative quantification. The treatment with chronic nicotine for 3 months led to moderate changes in the levels of endogenous dorsal striatum peptides. Five enkephalin opioid peptides were up-regulated, although no change was observed for dynorphin peptides. Specially, nicotine altered levels of nine non-opioid peptides derived from precursors, including somatostatin and cerebellin, which potentially modulate neurotransmitter release and energy metabolism. This broad but selective impact on the multiple peptidergic systems suggests that apart from the opioid peptides, several other peptidergic systems are involved in the preoccupation/craving phase of drug dependence. Our finding permits future evaluation of the neurochemical circuits modulated by chronic nicotine exposure and provides a number of novel molecules that could serve as potential therapeutic targets for treating drug dependence. Molecular & Cellular

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“…SST is a regulatory peptide originally discovered as the hypothalamic factor inhibiting growth hormone release [16,107] and subsequently found to have wide distribution and multiple functions in the brain [34,112]. SST acts via six subtypes of G-protein-coupled receptors, of which SSTR2(a) is one of the most abundant in the brain [54,112,101].…”

Section: Introductionmentioning

confidence: 99%

Critical role of somatostatin receptor 2 in the vulnerability of the central noradrenergic system: new aspects on Alzheimer’s disease

et al. 2015

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Alzheimer's disease and other age-related neurodegenerative disorders are associated with deterioration of the noradrenergic locus coeruleus (LC), a probable trigger for mood and memory dysfunction. LC noradrenergic neurons exhibit particularly high levels of somatostatin binding sites. This is noteworthy since cortical and hypothalamic somatostatin content is reduced in neurodegenerative pathologies. Yet the role of a somatostatin signal-

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Somatostatinergic systems in brain: Networks and functions

Cited by 179 publications

References 115 publications

MOLECULAR EVOLUTION OF GPCRS: Somatostatin/urotensin II receptors

MOLECULAR EVOLUTION OF GPCRS: Somatostatin/urotensin II receptors

Chronic Nicotine Treatment Impacts the Regulation of Opioid and Non-opioid Peptides in the Rat Dorsal Striatum

Critical role of somatostatin receptor 2 in the vulnerability of the central noradrenergic system: new aspects on Alzheimer’s disease

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