Somatostatin28(15–28), but not somatostatin28(1–12), affects central monoaminergic neurotransmission in rats

Vécsei, László; Widerlöv, Erik; Alling, Christer; Zsigo, Jozsef; Pávó, Imre; Penke, Botond

doi:10.1016/0143-4179(90)90060-c

Cited by 14 publications

(4 citation statements)

References 29 publications

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“…Since somatostatin can inhibit both presynaptic and postsynaptic sites, it may then directly modulate mitral cell‐granule cell synaptic interactions, and consequently alter the resulting oscillatory dynamics (Lagier et al,2004). The EPL is also innervated by feedback centrifugal fibers, including cholinergic, serotoninergic, or noradrenergic inputs (Shipley and Ennis,1996; Shepherd,2004) and somatostatin is known to influence monoaminergic release in many brain regions (Garcia‐Sevilla et al,1978; Göthert,1980; Tanaka and Tsujimoto,1981; Beal and Martin,1984; Vécsei et al,1990; Hathway et al,1998). Since peptides can act on synapses distant from their release sites, a putative action of somatostatin on such neuromodulatory elements cannot be ruled out.…”

Section: Discussionmentioning

confidence: 99%

Retinal vascular changes after glial disruption in rats

Shen¹,

Li²,

Chung³

et al. 2009

J of Neuroscience Research

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Glial dysfunction is found in a number of retinal vascular diseases but its link with blood-retinal barrier (BRB) breakdown remains poorly understood. The present study tested the hypothesis that glial dysfunction is a major contributor to the BRB breakdown that is a hallmark of retinal vascular diseases. We investigated the specificity of the purportedly selective glial toxin, DL-alpha-aminoadipic acid (DL-alpha-AAA) on different types of ocular cells in vitro and then tested the effect of glial disruption on retinal vasculature after intraocular injection of DL-alpha-AAA or siRNA targeting glutamine synthetase (GS) in rats. DL-alpha-AAA was toxic to astrocytes and Müller cells but not to other types of BRB-related cells in vitro. Subretinal injection of DL-alpha-AAA disrupted retinal glial cells, induced vascular telangiectasis and increased vascular permeability from 4 days to over 2 months post-injection. Vascular changes induced by DL-alpha-AAA were observed predominantly in regions of glial disruption, as reflected by reduced expression of GS and increased expression of glial fibrillary acidic protein and vimentin. Confocal microscopy showed changes in all three layers of the retinal vasculature, which co-localised with areas of Müller cell disruption. Double labeling immunohistochemistry revealed that retinal glial disruption after DL-alpha-AAA injection was accompanied by increased expression of vascular endothelial growth factor and reduced expression of the tight junction protein claudin-5. Intravitreal injection of GS siRNA induced similar changes in Müller cells and BRB breakdown. Our data are consistent with the hypothesis that glial dysfunction is a primary contributor to the BRB breakdown in retinal vascular diseases.

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Section: Discussionmentioning

confidence: 99%

Retinal vascular changes after glial disruption in rats

Shen¹,

Li²,

Chung³

et al. 2009

J of Neuroscience Research

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show abstract

“…Since somatostatin can inhibit both presynaptic and postsynaptic sites, it may then directly modulate mitral cellgranule cell synaptic interactions, and consequently alter the resulting oscillatory dynamics (Lagier et al, 2004). The EPL is also innervated by feedback centrifugal fibers, including cholinergic, serotoninergic, or noradrenergic inputs (Shipley and Ennis, 1996;Shepherd, 2004) and somatostatin is known to influence monoaminergic release in many brain regions (Garcia-Sevilla et al, 1978;Göthert, 1980;Tanaka and Tsujimoto, 1981;Beal and Martin, 1984;Vécsei et al, 1990;Hathway et al, 1998). Since peptides can act on synapses distant from their release sites, a putative action of somatostatin on such neuromodulatory elements cannot be ruled out.…”

Section: Somatostatin Release and Olfactory Processingmentioning

confidence: 98%

Somatostatin interneurons delineate the inner part of the external plexiform layer in the mouse main olfactory bulb

Lepousez

Csaba

Bernard

et al. 2010

J of Comparative Neurology

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Neuropeptides play a major role in the modulation of information processing in neural networks. Somatostatin, one of the most concentrated neuropeptides in the brain, is found in many sensory systems including the olfactory pathway. However, its cellular distribution in the mouse main olfactory bulb (MOB) is yet to be characterized. Here we show that approximately 95% of mouse bulbar somatostatin-immunoreactive (SRIF-ir) cells describe a homogeneous population of interneurons. These are restricted to the inner lamina of the external plexiform layer (iEPL) with dendritic field strictly confined to the region. iEPL SRIF-ir neurons share some morphological features of Van Gehuchten short-axon cells, and always express glutamic acid decarboxylase, calretinin, and vasoactive intestinal peptide. One-half of SRIF-ir neurons are parvalbumin-ir, revealing an atypical neurochemical profile when compared to SRIF-ir interneurons of other forebrain regions such as cortex or hippocampus. Somatostatin is also present in fibers and in a few sparse presumptive deep short-axon cells in the granule cell layer (GCL), which were previously reported in other mammalian species. The spatial distribution of somatostatin interneurons in the MOB iEPL clearly outlines the region where lateral dendrites of mitral cells interact with GCL inhibitory interneurons through dendrodendritic reciprocal synapses. Symmetrical and asymmetrical synaptic contacts occur between SRIF-ir dendrites and mitral cell dendrites. Such restricted localization of somatostatin interneurons and connectivity in the bulbar synaptic network strongly suggest that the peptide plays a functional role in the modulation of olfactory processing.

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“…At a behavioral level, SST 14 and SST 28 have been implicated in locomotion (Semenova et al 2010), analgesia (Williams et al 1987), epilepsy (Vécsei et al 1990), spatial memory (Dutar et al 2002), and emotion (Engin et al 2008). Engin et al found that intracerebroventricular (ICV) microinfusions of either SST 14 or a selective sst2 agonist produced significant reductions in rat 'anxiety' in the elevated plus maze (Engin et al 2008;Engin and Treit 2009).…”

Section: Introductionmentioning

confidence: 99%

Anxiolytic-like effects of somatostatin isoforms SST 14 and SST 28 in two animal models (Rattus norvegicus) after intra-amygdalar and intra-septal microinfusions

2011

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SST receptors in the septum and amygdala are responsive to both SST 14 and SST 28, but not those in the striatum. Although no obvious differences in the anxiolytic-like effects of the isoforms were detected, quantitative or even qualitative differences in their specific anxiolytic effects may occur in different sub-regions of the septum and amygdala, as has been found for benzodiazepine anxiolytics.

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Somatostatin28(15–28), but not somatostatin28(1–12), affects central monoaminergic neurotransmission in rats

Cited by 14 publications

References 29 publications

Retinal vascular changes after glial disruption in rats

Retinal vascular changes after glial disruption in rats

Somatostatin interneurons delineate the inner part of the external plexiform layer in the mouse main olfactory bulb

Anxiolytic-like effects of somatostatin isoforms SST 14 and SST 28 in two animal models (Rattus norvegicus) after intra-amygdalar and intra-septal microinfusions

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