Somatostatin modulates dopamine release in rat retina

The aim of the present study was to determine the possible role of somatostatin as a modulator of dopamine release in rat retina. Basal release of dopamine, and how this is influenced by somatostatin receptor (sst) selective ligands, was examined ex vivo in rat retinal explants. Dopamine levels were quantified by high-pressure liquid chromatography (HPLC) with electrochemical detection. Basal levels of dopamine were measured over 120 min of tissue incubation and found to be 1.17 ± 0.35 ng/ml. Somatostatin (10 -6, 10-5, 10-4 M) increased dopamine levels in a concentration-dependent manner, while the sst2 antagonist CYN154806 (10-4 M) reversed its actions. BIM23014 (sst2 agonist) increased dopamine levels in a statistically significant manner only at the concentration of 10-5 M. The sst1 agonist L797.591 (10-5, 10-4 M) also increased dopamine levels, while activation of the sst3 receptor (sst3 agonist, L796.778, 10-4 M) had no effect. These data substantiate a neuromodulatory role for sst1 and sst2 somatostatin receptors in the retina and show for the first time somatostatin's influence on dopamine release. © 2005 Elsevier Ireland Ltd. All rights reserved

Morphine cross-reacts with somatostatin receptor SSTR2 in the T47D human breast cancer cell line and decreases cell growth.

International audienceIn a previous study, we found that morphine decreases, in a dose-dependent manner, the cell growth of T47D human breast cancer cells, despite the lack of mu opioid receptors and an interaction of morphine with other opioid sites. We have therefore examined a possible interaction of morphine with other membrane receptor systems of the cell. The present study describes for the first time an interaction between mu-acting opioid drugs and the somatostatinergic system. We have found that [125I]Tyr11-somatostatin binds with high affinity to T47D cells. Analysis of the binding data showed the presence of two components: one with high affinity but low capacity (Kd, 0.145 nM; 1450 sites/cell), and another of lower affinity but higher capacity (Kd, 1.192 nM; 11920 sites/cell). Somatostatin-14 and somatostatin-28 showed multiphasic displacement curves, indicating heterogeneity of binding sites. The latter was confirmed by reverse transcription-PCR, which revealed the existence of the somatostatin receptor subtypes 2 and 3 (SSTR2 and SSTR3), with a relative mRNA concentration of 85 and 15%, respectively. Morphine and the morphinomimetic peptide morphiceptine (Tyr-Pro-Phe-Pro-NH2) displace somatostatin from its binding sites. Further analysis indicated that mu-acting opioids interact with the SSTR2 receptor subtype

Oral ulceration with bone sequestration: Retrospective study of eight cases and literature review

Objective: Oral ulceration with bone sequestration (OUBS) describes a site-specific intraoral ulcer that covers exposed, non-vital bone in patients lacking any etiological factor known to induce osteonecrosis. We aimed to conduct a retrospective study of eight new cases of OUBS and review the literature. Subjects and Methods: This is a retrospective study of OUBS cases, diagnosed and managed during 2007–2017. Inclusion criteria were the presence of oral ulcer with exposed non-vital bone at sites of bone prominence and the absence of any factor known to cause osteonecrosis. The English literature was reviewed on original OUBS cases. Results: Eight patients (5 males and 3 females, aged 27–75 years) were diagnosed with OUBS during years 2007–2017. Four cases involved the mandibular mylohyoid ridge, one a mandibular anterior exostosis and three the maxillary buccal/palatal exostoses. Exposed bone was removed under local anesthesia, resulting in complete healing in all cases. The literature review yielded 32 OUBS cases in the mandible. Conclusion: Oral ulceration with bone sequestration is a distinct, probably under-reported rather than rare clinical entity that should be regarded the provisional diagnosis in case of an oral ulcer covering exposed, non-vital bone at sites of bone prominence in patients lacking any etiological factor known to induce osteonecrosis. © 2018 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd. All rights reserve

Antidepressants influence somatostatin levels and receptor pharmacology in brain

This study investigated how the administration (acute and chronic) of the antidepressants citalopram and desmethylimipramine (DMI) influences somatostatin (somatotropin release inhibitory factor, SRIF) levels and SRIF receptor density (sst1-5) in rat brain. Animals received either of the following treatments: (1) saline for 21 days (control group), (2) saline for 20 days and citalopram or DMI for 1 day (citalopram or DMI acute groups), (3) citalopram or DMI for 21 days (citalopram or DMI chronic groups). Somatostatin levels were determined by radioimmunoassay. [125I]LTT SRIF-28 binding in the absence (labeling of sst1-5) or presence of 3 nM MK678 (labeling of sst1/4) and [125I]Tyr3 octreotide (labeling of sst2/5) binding with subsequent autoradiography was performed in brains of rats treated with both antidepressants. Somatostatin levels were increased after citalopram, but not DMI administration, in the caudate-putamen, hippocampus, nucleus accumbens, and prefrontal cortex. Autoradiography studies illustrated a significant decrease in receptor density in the superficial and deep layers of frontal cortex (sst2), as well as a significant increase in the CA1 (sst1/4) hippocampal field in brains of chronically citalopram-treated animals. DMI administration increased sst 1/4 receptors levels in the CA1 hippocampal region. These results suggest that citalopram and to a lesser extent DMI influence the function of the somatostatin system in brain regions involved in the emotional, motivational, and cognitive aspects of behavior. © 2009 Nature Publishing Group All rights reserved

The immunohistochemical profile of basal cell nevus syndrome–associated and sporadic odontogenic keratocysts: a systematic review and meta-analysis

Objectives: To provide a systematic review of the literature on studies comparing the immunoprofile of nevoid basal cell carcinoma syndrome (BCNS)–associated and sporadic odontogenic keratocysts (OKCs), in order to identify markers that could accurately distinguish the two OKC subtypes. Materials and methods: We searched MEDLINE/Pubmed, Web of Science, EMBASE via OVID, and grey literature for publications until December 28th, 2019, that compared the immunohistochemical expression of the two OKC subtypes. The studies were qualitatively assessed using the Critical Appraisal Tool for Case Series (Joana Briggs Institute). Sensitivity and specificity, positive and negative likelihood ratio, diagnostic odds ratio and area under the curve, and pooled estimates were calculated, using a random-effects model. Results: Seventy-one studies were qualitatively analyzed; 61 markers were evaluated in one study and 32 in ≥ 2 studies. Twenty-five studies reported differential expression of 29 markers in the form of higher number of positive cells or greater staining intensity usually in BCNS-associated OKCs. Meta-analysis for bcl-2, Cyclin D1, CD56, CK18, p53, and PCNA showed that none of those markers is distinguishable between BCNS-associated and sporadic OKCs, in a 95% confidence interval. The risk of bias was high in 34 studies, moderate in 22, and low in 15. Conclusions: The present systematic review and meta-analysis uncovered that, although several immunohistochemical markers might characterize the OKC phenotype, they cannot discriminate between the BCNS-associated and sporadic OKCs. Clinical relevance: This study highlighted the requirement for additional screening for markers by immunohistochemistry, preferentially coupled to alternative diagnostic applications such as genomics technologies. © 2021, The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature

Antidepressants influence somatostatin levels and receptor pharmacology in brain

This study investigated how the administration (acute and chronic) of the antidepressants citalopram and desmethylimipramine (DMI) influences somatostatin (somatotropin release inhibitory factor, SRIF) levels and SRIF receptor density (sst1-5) in rat brain. Animals received either of the following treatments: (1) saline for 21 days (control group), (2) saline for 20 days and citalopram or DMI for 1 day (citalopram or DMI acute groups), (3) citalopram or DMI for 21 days (citalopram or DMI chronic groups). Somatostatin levels were determined by radioimmunoassay. [125I]LTT SRIF-28 binding in the absence (labeling of sst1-5) or presence of 3 nM MK678 (labeling of sst1/4) and [125I]Tyr3 octreotide (labeling of sst2/5) binding with subsequent autoradiography was performed in brains of rats treated with both antidepressants. Somatostatin levels were increased after citalopram, but not DMI administration, in the caudate-putamen, hippocampus, nucleus accumbens, and prefrontal cortex. Autoradiography studies illustrated a significant decrease in receptor density in the superficial and deep layers of frontal cortex (sst2), as well as a significant increase in the CA1 (sst1/4) hippocampal field in brains of chronically citalopram-treated animals. DMI administration increased sst 1/4 receptors levels in the CA1 hippocampal region. These results suggest that citalopram and to a lesser extent DMI influence the function of the somatostatin system in brain regions involved in the emotional, motivational, and cognitive aspects of behavior. © 2009 Nature Publishing Group All rights reserved