Sustained stress-induced changes in mice as a model for chronic depression

Elizalde, N.; Garcia-García, Álvaro L.; Totterdell, Susan; Gendive, Nerea; Venzala, E.; Ramı́rez, Marı́a J.; Rı́o, Joaquı́n Del; Tordera, Rosa M.

doi:10.1007/s00213-010-1835-6

Cited by 91 publications

(62 citation statements)

References 65 publications

(80 reference statements)

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“…It will be important to identify the proteins that are up regulated in c-Fos-ir neurons after caffeine administration. It has been shown that repeated stress or chronic stress results in less c-Fos expression (Badowska-Szalewska et al 2006;Girotti et al 2006;Elizalde et al 2010). Correspondingly, we identified that repeated doses of caffeine result in an attenuation of c-Fos protein expression.…”

Section: Discussionsupporting

confidence: 65%

“…Our data showing that the repeated and chronic effect of caffeine attenuates signal transcription in the immediate early gene-mediated pathway agrees with the data of Svenningsson and Fredholm (1997) who showed that repeated administration of caffeine reduces c-fos mRNA expression in the globus pallidus. Moreover, chronic stress induced the down-regulation of glutamic acid decarboxylase-65 (GAD65) and vesicular glutamate transporter1 (vGlut1) expression (Elizalde et al 2010). We suggest that repeated doses of caffeine suppress either adenosine receptor expression or glutamate receptor expression.…”

Section: Discussionmentioning

confidence: 98%

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Regulation of Neuronal Activation by Alpha2A Adrenergic Receptor Agonist

Savchenko

Boughter

2010

Neurotox Res

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Stress factors induce neuronal activation in brain areas that are related to anxiety and fear. High doses of caffeine induce neuronal activation with Ca2+ influx followed by expression of the immediate early gene c-fos. In the present study, we investigated c-Fos protein expression in stress-responsive brain areas induced by caffeine, as well as the role of alpha2A receptor in the regulation of neuronal activation. Immunohistochemical analysis showed that an acute effect of caffeine induced c-Fos protein expression in the hippocampus, the bed nucleus of stria terminalis (BNST), the lateral septum, the basolateral and central amygdala, the paraventricular hypothalamic nucleus (PVN), the locus coeruleus, and the lateral parabrachial nucleus (LPBN). However, c-Fos expression was attenuated after repeated treatment of caffeine, spaced 24 h apart, compared to a single acute effect. Alpha2A receptor activation with the agonist guanfacine attenuated the acute effect of caffeine in terms of c-Fos expression in neurons in the CA1-CA3 areas of hippocampus, the locus coeruleus and the LPBN as compared with effect of caffeine alone, whereas the number of c-Fos expressing neurons increased in the lateral septum, the dorsal BNST, the central amygdala, and the PVN, areas that are densely innervated by noradrenergic neurons. Guanfacine alone induced c-Fos protein expression in neurons in the central amygdala, the dorsal BNST, the PVN, the LPBN, and the caudal nucleus of the solitary tract. Guanfacine alone also induced phosphorylation of extracellular signal-regulated kinase 1/2 (ERK1/2) in neurons expressing c-Fos in the dorsal BNST, the central amygdala, and the LPBN. These results suggest that alpha2A receptor activation modulates synaptic transmission in neuronal circuits that are correlated with stress in vivo.

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Section: Discussionsupporting

confidence: 65%

Section: Discussionmentioning

confidence: 98%

Regulation of Neuronal Activation by Alpha2A Adrenergic Receptor Agonist

Savchenko

Boughter

2010

Neurotox Res

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“…Consistent with previous reports (Briones et al 2012;Elizalde et al 2010), the present study shows that depressive phenotype of anhedonia is observed as later as 7 weeks in Wistar rats, which is not in agreement with previous observations in Lister hooded or Sprague Dawley rats (D'Aquila et al 1994;Grønli et al 2004). This disagreement may be related to different animal strains (Lister hooded or Sprague Dawley versus Wistar rats) and sucrose dose (1 % versus 2 %).…”

Section: Discussionsupporting

confidence: 55%

“…Also, CMS was shown to downregulate expression of BDNF and activation of cAMP-response element binding protein (CREB), both involved in the pathophysiology of depression and the mechanism of action of antidepressants (Hu et al 2010). CMS was also shown to suppress adult hippocampal cytogenesis, which has been suggested to play a role in depression (Elizalde et al 2010;Schoenfeld and Cameron 2015).…”

Section: Introductionmentioning

confidence: 98%

Piromelatine ameliorates memory deficits associated with chronic mild stress-induced anhedonia in rats

Xie

Laudon

et al. 2016

Psychopharmacology

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“…In support of this theory, a study on the role of SNCA showed a significant decrease in the frequency of miniature excitatory postsynaptic potentials in mice overexpressing human SNCA (68). Furthermore, the decrease in hippocampal GABA levels seen in studies on mice exposed to CMS could also be explained by a deficit in vesicular function (69,70).…”

Section: Discussionmentioning

confidence: 58%

Candidate Hippocampal Biomarkers of Susceptibility and Resilience to Stress in a Rat Model of Depression

Henningsen

Palmfeldt

Christiansen

et al. 2012

Molecular & Cellular Proteomics

105

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Susceptibility to stress plays a crucial role in the development of psychiatric disorders such as unipolar depression and post-traumatic stress disorder. In the present study the chronic mild stress rat model of depression was used to reveal stress-susceptible and stress-resilient rats. Largescale proteomics was used to map hippocampal protein alterations in different stress states. Membrane proteins were successfully captured by two-phase separation and peptide based proteomics. Using iTRAQ labeling coupled with mass spectrometry, more than 2000 proteins were quantified and 73 proteins were found to be differentially expressed. Stress susceptibility was associated with increased expression of a sodium-channel protein (SCN9A) currently investigated as a potential antidepressant target. Differential protein profiling also indicated stress susceptibility to be associated with deficits in synaptic vesicle release involving SNCA, SYN-1, and AP-3. Our results indicate that increased oxidative phosphorylation (COX5A, NDUFB7, NDUFS8, COX5B, and UQCRB) within the hippocampal CA regions is part of a stress-protection mechanism.

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Sustained stress-induced changes in mice as a model for chronic depression

Abstract: This study shows region-specific long-term neurobiological adaptations induced by CMS and residual hippocampal signs after paroxetine treatment. We propose the use of this model to study molecular mechanisms involved in chronic depression and vulnerability for relapse.

Cited by 91 publications

References 65 publications

Regulation of Neuronal Activation by Alpha2A Adrenergic Receptor Agonist

Regulation of Neuronal Activation by Alpha2A Adrenergic Receptor Agonist

Piromelatine ameliorates memory deficits associated with chronic mild stress-induced anhedonia in rats

Candidate Hippocampal Biomarkers of Susceptibility and Resilience to Stress in a Rat Model of Depression

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