Chronic mild stress alters the somatostatin receptors in the rat brain

Faron-Górecka, Agata; Kuśmider, Maciej; Kolasa, Magdalena; Żurawek, Dariusz; Szafran-Pilch, Kinga; Gruca, Piotr; Pabian, Paulina; Solich, Joanna; Papp, Mariusz; Dziedzicka-Wasylewska, Marta

doi:10.1007/s00213-015-4103-y

Cited by 30 publications

(19 citation statements)

References 63 publications

(78 reference statements)

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“…Such an assumption is also supported by studies, in which the binding of this radioligand was not detected in SST 2 R knockout mice (Hannon et al 2002). In agreement with our previous studies (Faron-Górecka et al 2016), a high density of SST receptors was observed in the control and stressed or/and imipramine treatment groups using [ 125 I]Tyr3-Octreotide binding in different brain areas. Representative autoradiograms are presented in Fig.…”

Section: Resultssupporting

confidence: 92%

“…Following this experimental paradigm, increased [ 125 I]Tyr 3 -Octreotide binding was observed in all brain regions involved in the stress reaction. These results are contrary to the effect of a shorter period of the CMS protocol (2 weeks), which resulted in a decrease in sst 2 R binding in the studied brain regions (with the exception of the MHb, where an increase in sst 2 R binding was observed, Faron-Górecka et al 2016). However, the opposing effects of 2 and 7 weeks of the CMS protocol are not surprising.…”

Section: Discussioncontrasting

confidence: 72%

“…In our previously published studies, we have demonstrated a significant negative correlation between basal prolactin levels (i.e., before the CMS procedure) and the behavioural response to IMI administration (Faron-Górecka et al 2017). Recently, we also highlighted the role of sst 2 R in the stress reaction (Faron-Górecka et al 2016; Faron-Górecka & Szafran-Pilch 2016). In the present study, we investigated the role of sst 2 R in response to IMI treatment following an extended period (7 weeks) of the CMS protocol.…”

Section: Discussionmentioning

confidence: 91%

“…Additionally, the increased expression of the mRNA-encoding sst 2 R within the amygdala and anterior cingulate cortex in the predator stress model has been observed (Nanda et al 2008). In our previously published work, we demonstrated the involvement of sst 2 R in response to 2 weeks of chronic unpredictable stress (CMS) in rats (Faron-Górecka et al 2016). …”

Section: Introductionmentioning

confidence: 95%

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Regulation of somatostatin receptor 2 in the context of antidepressant treatment response in chronic mild stress in rat

et al. 2018

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RationaleThe role of somatostatin and its receptors for the stress-related neuropsychiatric disorders has been widely raised. Recently, we have also demonstrated the involvement of somatostatin receptor type 2-sst2R and dopamine receptor type 2-D2R in stress.ObjectiveIn this context, we decided to find if these receptors are involved in response to antidepressant treatment in animal model of depression—chronic mild stress (CMS).MethodsHere, we report data obtained following 7-week CMS procedure. The specific binding of [125I]Tyr3-Octreotide to sst2R and [3H]Domperidone to D2R was measured in the rat brain, using autoradiography. Additionally, the level of dopamine and metabolites was measured in the rat brain.ResultsIn the final baseline test after 7 weeks of stress, the reduced consumption of sucrose solution was observed (controls vs the stressed animals (6.25 0.16 vs. 10.39 0.41; p < 0.05). Imipramine was administered for the next 5 weeks, and it reversed anhedonia in majority of animals (imipramine-reactive); however, in some animals, it did not (imipramine-non-reactive). Two-way repeated measures ANOVA revealed significant effects of stress and treatment and time interaction [F(16, 168) = 3.72; p < 0.0001], n = 10 per groups. We observed decreased binding of [125I]Tyr3-Octreotide in most of rat brain regions in imipramine non-reactive groups of animals. The decrease of D2R after stress in striatum and nucleus accumbens and no effect of imipramine were observed.In the striatum and prefrontal cortex, the significant role of stress and imipramine in dopamine levels was observed.ConclusionsThe results obtained in binding assays, together with dopamine level, indicate the involvement of sst2R receptors for reaction to antidepressant treatment. Besides, the stress context itself changes the effect of antidepressant drug.

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Section: Resultssupporting

confidence: 92%

Section: Discussioncontrasting

confidence: 72%

Section: Discussionmentioning

confidence: 91%

Section: Introductionmentioning

confidence: 95%

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Regulation of somatostatin receptor 2 in the context of antidepressant treatment response in chronic mild stress in rat

et al. 2018

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“…GAD1 mRNA 59,60 , PVALB mRNA 61 , and SST mRNA 62 signals correspond to previously described distributions. Although cortical SSTR2 mRNA signals were lighter in comparison to some studies 63 , the distribution corresponds to SSTR2 mRNA and SSTR2 binding results in multiple other studies (Supplementary Figure 1A) [64][65][66][67][68] . Control (sense) riboprobe hybridization, for all transcripts, was at background levels (Supplementary Figure 1B, 2).…”

Section: Resultsmentioning

confidence: 58%

Effect of Immune Activation during Early Gestation or Late Gestation on Inhibitory Markers in Adult Male Rats

Rahman

Weickert

Harms

et al. 2020

Sci Rep

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People with schizophrenia exhibit deficits in inhibitory neurons and cognition. The timing of maternal immune activation (MIA) may present distinct schizophrenia-like phenotypes in progeny. We investigated whether early gestation [gestational day (GD) 10] or late gestation (GD19) MIA, via viral mimetic polyI:C, produces deficits in inhibitory neuron indices (GAD1, PVALB, SST, SSTR2 mRNAs) within cortical, striatal, and hippocampal subregions of male adult rat offspring. In situ hybridisation revealed that polyI:C offspring had: (1) SST mRNA reductions in the cingulate cortex and nucleus accumbens shell, regardless of MIA timing; (2) SSTR2 mRNA reductions in the cortex and striatum of GD19, but not GD10, MIA; (3) no alterations in cortical or striatal GAD1 mRNA of polyI:C offspring, but an expected reduction of PVALB mRNA in the infralimbic cortex, and; (4) no alterations in inhibitory markers in hippocampus. Maternal IL-6 response negatively correlated with adult offspring SST mRNA in cortex and striatum, but not hippocampus. These results show lasting inhibitory-related deficits in cortex and striatum in adult offspring from MIA. SST downregulation in specific cortical and striatal subregions, with additional deficits in somatostatin-related signalling through SSTR2, may contribute to some of the adult behavioural changes resulting from MIA and its timing. Neural activity between the cortex and striatum regulates motor, cognitive, and limbic function, and aspects of these modalities are perturbed in people with schizophrenia 1,2. This neural activity is influenced by local inhibitory neurons, and the dysregulation of inhibition is postulated as a central contributor in the development of schizophrenia. Inhibitory tone is mainly established during early neurodevelopment to coordinate efficient neurotransmission 3,4. Inhibitory interneurons migrate from the ganglionic eminence and the subventricular zone through the white matter to reach their destination in the cortical grey matter (see 5 for review) and hippocampus (see 6 for review). Striatal neurons are largely generated from the ganglionic eminences 7. Perturbations during this neurodevelopmental epoch is therefore postulated to dysregulate inhibitory tone in the brain 8 and contribute to the behavioural phenotypes in schizophrenia (see 9,10 for review). Glutamate decarboxylase-1 (GAD1) is one of the enzymes that catalyses the main inhibitory neurotransmitter in the brain, gamma-aminobutyric acid (GABA) 11. There are two main subsets of GABAergic neurons that are distinguished based on their expression of the calcium-binding protein, parvalbumin (PVALB), or the neuropeptide hormone, somatostatin (SST) (see 12 for review). Studies in post-mortem human brain show that schizophrenia cases have reduced cortical 13 , hippocampal 14,15 , and striatal 16,17 GABAergic indices that suggest that these regions may contribute to the cognitive deficits exhibited by people with schizophrenia. The most consistently reported inhibitory deficits in the cortex of people with s...

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Chronic mild stress paradigm as a rat model of depression: facts, artifacts, and future perspectives

et al. 2022

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Rationale The chronic mild stress (CMS) paradigm was first described almost 40 years ago and has become a widely used model in the search for antidepressant drugs for major depression disorder (MDD). It has resulted in the publication of almost 1700 studies in rats alone. Under the original CMS procedure, the expression of an anhedonic response, a key symptom of depression, was seen as an essential feature of both the model and a depressive state. The prolonged exposure of rodents to unpredictable/uncontrollable mild stressors leads to a reduction in the intake of palatable liquids, behavioral despair, locomotor inhibition, anxiety-like changes, and vegetative (somatic) abnormalities. Many of the CMS studies do not report these patterns of behaviors, and they often fail to include consistent molecular, neuroanatomical, and physiological phenotypes of CMS-exposed animals. Objectives To critically review the CMS studies in rats so that conceptual and methodological flaws can be avoided in future studies. Results Analysis of the literature supports the validity of the CMS model and its impact on the field. However, further improvements could be achieved by (i) the stratification of animals into ‘resilient’ and ‘susceptible’ cohorts within the CMS animals, (ii) the use of more refined protocols in the sucrose test to mitigate physiological and physical artifacts, and (iii) the systematic evaluation of the non-specific effects of CMS and implementation of appropriate adjustments within the behavioral tests. Conclusions We propose methodological revisions and the use of more advanced behavioral tests to refine the rat CMS paradigm, which offers a valuable tool for developing new antidepressant medications.

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Chronic mild stress alters the somatostatin receptors in the rat brain

Cited by 30 publications

References 63 publications

Regulation of somatostatin receptor 2 in the context of antidepressant treatment response in chronic mild stress in rat

Regulation of somatostatin receptor 2 in the context of antidepressant treatment response in chronic mild stress in rat

Effect of Immune Activation during Early Gestation or Late Gestation on Inhibitory Markers in Adult Male Rats

Chronic mild stress paradigm as a rat model of depression: facts, artifacts, and future perspectives

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