Distribution and characterisation of somatostatin receptor mRNA and binding sites in the brain and periphery

Fehlmann, Dominique; Langenegger, Daniel; Schuepbach, E.; Siehler, Sandra; Feuerbach, Dominik; Hoyer, Daniel

doi:10.1016/s0928-4257(00)00208-4

Cited by 80 publications

(67 citation statements)

References 37 publications

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“…1 The pharmacological characterization of the receptors involved as sst5 type may seem surprising. Based on morphological results, the presence of receptors of the sst5 type in some central nervous system regions is in fact controversial (Fehlmann et al, 2000;Rocheville et al, 2000a;Schulz et al, 2000;Kang et al, 2003). We therefore analyzed proteins from purified synaptosomal membranes for the presence of the sst5 receptor protein.…”

Section: Resultsmentioning

confidence: 99%

Somatostatin-Induced Activation and Up-Regulation of N-Methyl-d-aspartate Receptor Function: Mediation through Calmodulin-Dependent Protein Kinase II, Phospholipase C, Protein Kinase C, and Tyrosine Kinase in Hippocampal Noradrenergic Nerve Endings

Pittaluga¹,

Feligioni²,

Longordo³

et al. 2004

J Pharmacol Exp Ther

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Somatostatin receptors and glutamate N-methyl-D-aspartate(NMDA) receptors coexist on hippocampal noradrenergic axon terminals. Activation of somatostatin receptors was previously found to positively influence the function of NMDA receptors regulating norepinephrine release. The somatostatin receptors involved were pharmacologically characterized as sst5 type in experiments in Mg 2ϩ -free solutions. Here, we first confirm the pharmacology of these receptors using selective sst5 ligands in Mg 2ϩ -containing solutions. Moreover, we show by Western blot that the sst5 protein exists on purified hippocampal synaptosomal membranes. We then investigated the pathways connecting the two receptors using as a functional response the release of norepinephrine from rat hippocampal synaptosomes in superfusion. The release of norepinephrine evoked by somatostatin-14 plus NMDA/glycine was partly prevented by the protein kinase C in- Glutamate N-methyl-D-aspartate (NMDA) receptors are ion channel-associated receptors expressed by coassembly of NR1 and NR2(A-D) subunits. These receptors display both pre-and postsynaptic localization and play relevant roles in development, neuroplasticity, and excitotoxicity (for review,

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Section: Resultsmentioning

confidence: 99%

Somatostatin-Induced Activation and Up-Regulation of N-Methyl-d-aspartate Receptor Function: Mediation through Calmodulin-Dependent Protein Kinase II, Phospholipase C, Protein Kinase C, and Tyrosine Kinase in Hippocampal Noradrenergic Nerve Endings

Pittaluga¹,

Feligioni²,

Longordo³

et al. 2004

J Pharmacol Exp Ther

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“…The study showed expression of all five ssts in the brain and pituitary, whereas other investigated organs, e.g., lungs, liver, and pancreas, varied in their tissue sst expression. The mRNAs for all five ssts were also detected in mouse brain (Fehlmann et al 2000) and in the retina (Cristiani et al 2002), whereas only sst [3][4][5] were expressed in the kidney (Bates et al 2003). However, to elucidate the more exact cellular distribution of sst, immunohistochemical (IHC) investigations are needed.…”

mentioning

confidence: 99%

Expression and Distribution of Somatostatin Receptor Subtypes in the Pancreatic Islets of Mice and Rats

Ludvigsen

Olsson

Stridsberg³

et al. 2004

J Histochem Cytochem.

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S U M M A R Y Somatostatin acts on specific membrane receptors (sst [1][2][3][4][5] ) to inhibit exocrine and endocrine functions. The aim was to investigate the distribution of sst [1][2][3][4][5] in pancreatic islet cells in normal mice and rats. Pancreatic samples from five adult C57BL/6 mice and Sprague-Dawley rats were stained with antibodies against sst 1-5 and insulin, glucagon, somatostatin, or pancreatic polypeptide (PP). A quantitative analysis of the co-localization was performed. All ssts were expressed in the pancreatic islets and co-localized on islet cells to various extents. A majority of the ␤ -cells expressed sst 1-2 and sst 5 in mouse islets, while Յ 50% in the rat expressed sst [1][2][3][4][5] . The expression of sst 1-5 on ␣ -cells did not differ much among species, with sst 2 and sst 5 being highly expressed. About 70% of the ␦ -cells expressed sst 1-4 in the rat pancreas, whereas 50% of the islet cells expressed sst 1-5 in the mouse. Furthermore, 60% of the PP-cells expressed sst [1][2][3][4][5] in the mouse, while the rat islets had lower values. Co-expression with the four major islet hormones varies among species and sst subtypes. These similarities and differences are interesting and need further evaluation to elucidate their physiological role in islets.

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“…SRIF receptors have been localized in the abovementioned brain regions (Fehlmann et al, 2000;Schulz et al, 2000). With the cloning of the SRIF receptors , tools have become available to study the presence of each receptor subtype.…”

Section: Discussionmentioning

confidence: 99%

“…Brains were cut at 10 mm sections. Receptor autoradiography was performed according to the following procedure (Fehlmann et al, 2000): after 20 min of preincubation in buffer containing 50 mM Tris-HCl, 2 mM EGTA, 5 mM MgCl 2 , 0.1 mM bacitracin, and 0.2% BSA (pH 7.4), at room temperature (RT), the sections were incubated for 2 h at RT in the same medium supplemented with 50 pM [ 125 I]LTT SRIF-28 in the absence (to label all SRIF receptors) or the presence of 3 nM MK678 (to label sst 1 and sst 4 receptors) or 50 pM [ 125 I]Tyr 3 octreotide (to label sst 2 and sst 5 receptors). Nonspecific binding was determined in a set of adjacent slides by incubation in the presence of 1 mM SRIF-28 (Tocris; Cookson Inc.).…”

Section: Receptor Autoradiography Studiesmentioning

confidence: 99%

Antidepressants Influence Somatostatin Levels and Receptor Pharmacology in Brain

Pallis

Vasilaki

Fehlmann

et al. 2008

Neuropsychopharmacol

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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 (sst 1-5 ) 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. [ 125 I]LTT SRIF-28 binding in the absence (labeling of sst 1-5 ) or presence of 3 nM MK678 (labeling of sst 1/4 ) and [ 125 I]Tyr 3 octreotide (labeling of sst 2/5 ) 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 (sst 2 ), as well as a significant increase in the CA1 (sst 1/4 ) 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.

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Distribution and characterisation of somatostatin receptor mRNA and binding sites in the brain and periphery

Cited by 80 publications

References 37 publications

Somatostatin-Induced Activation and Up-Regulation of N-Methyl-d-aspartate Receptor Function: Mediation through Calmodulin-Dependent Protein Kinase II, Phospholipase C, Protein Kinase C, and Tyrosine Kinase in Hippocampal Noradrenergic Nerve Endings

Somatostatin-Induced Activation and Up-Regulation of N-Methyl-d-aspartate Receptor Function: Mediation through Calmodulin-Dependent Protein Kinase II, Phospholipase C, Protein Kinase C, and Tyrosine Kinase in Hippocampal Noradrenergic Nerve Endings

Expression and Distribution of Somatostatin Receptor Subtypes in the Pancreatic Islets of Mice and Rats

Antidepressants Influence Somatostatin Levels and Receptor Pharmacology in Brain

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