The anxiolytic effects of somatostatin following intra-septal and intra-amygdalar microinfusions are reversed by the selective sst2 antagonist PRL2903

Yeung, Michelle; Treit, Dallas

doi:10.1016/j.pbb.2011.12.012

Cited by 36 publications

(26 citation statements)

References 28 publications

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“…Pharmacological experiments have revealed anxiolytic activity of SST after microinjections into ventricles, amygdala or septum [3,4]. In a previous study, SST deficient mice displayed only insignificant trends towards increased anxiety in the light/ dark- avoidance test, but details about time points of testing were not provided [11].…”

Section: Discussionmentioning

confidence: 99%

“…Evidence suggests that somatostatin (SST) is one neuropeptide with potent anxiolytic properties [3,4] and a role in fear memory formation [5], which may thus hold significant potential for the treatment of anxiety- and stress-related disorders [6]. …”

Section: Introductionmentioning

confidence: 99%

“…The anxiolytic activity of SST appears to be exerted at least in part via the amygdala [3,4], where it is endogenously expressed in a subpopulation of GABAergic interneurons with defined morphological and electrophysiological properties [7,8]. These interneurons form local microcircuits with the principal cells that are critically involved in the processing of fear- and anxiety-related information [9].…”

Section: Introductionmentioning

confidence: 99%

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Circadian Modulation of Anxiety: A Role for Somatostatin in the Amygdala

et al. 2013

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Pharmacological evidence suggests that the neuropeptide somatostatin (SST) exerts anxiolytic action via the amygdala, but findings concerning the putative role of endogenous SST in the regulation of emotional responses are contradictory. We hypothesized that an endogenous regulation of SST expression over the course of the day may determine its function and tested both SST gene expression and the behavior of SST knock out (SST-/-) mice in different aversive tests in relation to circadian rhythm. In an open field and a light/dark avoidance test, SST-/- mice showed significant hyperactivity and anxiety-like behavior during the second, but not during the first half of the active phase, failing to show the circadian modulation of behavior that was evident in their wild type littermates. Behavioral differences occurred independently of changes of intrinsically motivated activity in the home cage. A circadian regulation of SST mRNA and protein expression that was evident in the basolateral complex of the amygdala of wild type mice may provide a neuronal substrate for the observed behavior. However, fear memory towards auditory cue or the conditioning context displayed neither a time- nor genotype-dependent modulation. Together this indicates that SST, in a circadian manner and putatively via its regulation of expression in the amygdala, modulates behavior responding to mildly aversive conditions in mice.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Circadian Modulation of Anxiety: A Role for Somatostatin in the Amygdala

et al. 2013

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“…More advanced fixation techniques [43] Several clinical and experimental studies indicate that the SST system is also implicated in stress, anxiety and depression [64], and there is now direct evidence that, in fact, the receptor involved is SSTR2 [32,33,118]. Notably, depression is a leading neuropsychiatric complication in Alzheimer's disease [94], and an association with chronic life stress and laterlife cognitive dysfunction has been proposed [46].…”

Section: Attenuated Somatodendritic Inhibition and Dysfunctional Strementioning

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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“…36 Microinjections of SST into the amygdala or ventricles exert anxiolytic effects in the elevated plus maze test. 37,38 Reducing SST neuronal function acutely and chronically in the frontal cortex yields opposite effects on behavioral emotionality, suggesting that mood regulation may depend on complex network adaptations including multiple regions and on the timeframe. 39 In addition, it is not known whether HPA axis dysregulation of Sst KO mice contributes to these behavioral changes.…”

Section: Introductionmentioning

confidence: 99%

Somatostatin, neuronal vulnerability and behavioral emotionality

2015

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Somatostatin (SST) deficits are common pathological features in depression and other neurological disorders with mood disturbances, but little is known about the contribution of SST deficits to mood symptoms or causes of these deficits. Here we show that mice lacking Sst (SstKO) exhibit elevated behavioral emotionality, high basal plasma corticosterone and reduced gene expression of Bdnf, Cortistatin, and Gad67, together recapitulating behavioral, neuroendocrine and molecular features of human depression. Studies in SstKO and heterozygous (SstHZ) mice show that elevated corticosterone is not sufficient to reproduce the behavioral phenotype, suggesting a putative role for Sst cell-specific molecular changes. Using laser-capture microdissection, we show that cortical SST-positive interneurons display significantly greater transcriptome deregulations after chronic stress compared to pyramidal neurons. Protein translation through eukaryotic initiation factor 2 (EIF2) signaling, a pathway previously implicated in neurodegenerative diseases, was most affected and suppressed in stress-exposed SST neurons. We then show that activating EIF2 signaling through EIF2 kinase inhibition mitigated stress-induced behavioral emotionality in mice. Together, our data suggest that (1) low SST plays a causal role in mood-related phenotypes, (2) deregulated EIF2-mediated protein translation may represent a mechanism for vulnerability of SST neurons, and (3) that global EIF2 signaling has antidepressant/anxiolytic potential.

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The anxiolytic effects of somatostatin following intra-septal and intra-amygdalar microinfusions are reversed by the selective sst2 antagonist PRL2903

Cited by 36 publications

References 28 publications

Circadian Modulation of Anxiety: A Role for Somatostatin in the Amygdala

Circadian Modulation of Anxiety: A Role for Somatostatin in the Amygdala

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

Somatostatin, neuronal vulnerability and behavioral emotionality

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