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Effects of glutamate release inhibition on the transcriptome of BA-NAc neurons

ABSTRACT: Reduced reward interest/learning and reward-to-effort valuation are distinct, common symptoms in neuropsychiatric disorders for which chronic stress is a major aetiological factor. Pyramidal glutamate neurons in the basal amygdala (BA) project to various brain regions including nucleus accumbens (NAc). The BA-NAc neural pathway is activated by reward and aversion, with many neurons being monovalent. In adult male mice, chronic social stress (CSS) led to both reduced discriminative reward learning (DRL) associated with decreased BA-NAc Ca2+ activity, and reduced sucrose reward-to-effort valuation (REV) associated, in contrast, with increased BA-NAc Ca2+ activity. Chronic tetanus toxin inhibition of BA-NAc neurons replicated the CSS-DRL effect whilst causing only a mild REV reduction, whilst chronic DREADDs activation of BA-NAc neurons replicated the CSS effect on REV without affecting DRL. This study provides novel evidence that chronic stress disruption of reward processing involves the BA-NAc neural pathway; the bi-directional effects implicate activity changes in BA-NAc reward (learning) and aversion (effort) neurons, with the net overall direction of stress-induced change in activity dependent on on-going stimulus processing and behaviour.

ORGANISM(S): Mus musculus

PROVIDER: GSE216588 | GEO | 2022/12/01

REPOSITORIES: GEO

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Effects of Chronic Social Stress on the transcriptome of BA-NAc neurons

Project description:Reduced reward interest/learning and reward-to-effort valuation are distinct, common symptoms in neuropsychiatric disorders for which chronic stress is a major aetiological factor. Pyramidal glutamate neurons in the basal amygdala (BA) project to various brain regions including nucleus accumbens (NAc). The BA-NAc neural pathway is activated by reward and aversion, with many neurons being monovalent. In adult male mice, chronic social stress (CSS) led to both reduced discriminative reward learning (DRL) associated with decreased BA-NAc Ca2+ activity, and reduced sucrose reward-to-effort valuation (REV) associated, in contrast, with increased BA-NAc Ca2+ activity. Chronic tetanus toxin inhibition of BA-NAc neurons replicated the CSS-DRL effect whilst causing only a mild REV reduction, whilst chronic DREADDs activation of BA-NAc neurons replicated the CSS effect on REV without affecting DRL. This study provides novel evidence that chronic stress disruption of reward processing involves the BA-NAc neural pathway; the bi-directional effects implicate activity changes in BA-NAc reward (learning) and aversion (effort) neurons, with the net overall direction of stress-induced change in activity dependent on on-going stimulus processing and behaviour.

2022-12-01 | GSE216587 | GEO

Basal amygdala-nucleus accumbens glutamate neurons respond to either social reward or social aversion

Project description:A substantial proportion of basal amygdala (BA) glutamate neurons project to nucleus accumbens (NAc). The evidence that these neurons are activated by reward and/or aversion is equivocal. Social stimuli are highly salient, and in male mice we conducted a detailed analysis of the responsiveness of BA-NAc neurons to estrous female (social reward, SR) or aggressive male (social aversion, SA). Both SR and SA activated c-Fos expression in a relatively high number of BA-NAc neurons in intermediate (int) BA. Using Fos-TRAP2 mice, the majority of social int-BA-NAc neurons were activated by either SR or SA, i.e. were monovalent, and in similar numbers. Fiber photometry provided corroborative evidence that int-BA-NAc neural pathway activity was similar in response to SR or SA. These findings contribute substantially to understanding the topography and valence-specificity of BA-NAc neurons with respect to highly salient stimuli, and to identifying molecular targets for treatment of reward- or aversion-specific psychopathologies.

2023-12-17 | GSE220269 | GEO

Distinct reward processing by subregions of the nucleus accumbens

Project description:The nucleus accumbens (NAc) plays an important role in motivation and reward processing. Recent studies suggest that different NAc subnuclei differentially contribute to reward-related behaviors. However, how reward is encoded in individual NAc neurons remains unclear. Using in vivo single-cell resolution calcium imaging, we discovered diverse patterns of reward encoding in the medial and lateral shell subdivision of the NAc (NAcMed and NAcLat, respectively). Reward consumption increases NAcLat activity but decreases NAcMed activity, albeit with high variability among neurons. The heterogeneity in reward encoding could be attributed to differences in their synaptic inputs and transcriptional profiles. Specific optogenetic activation of Nts-positive neurons in the NAcLat promotes positive reinforcement, while activation of Cartpt-positive neurons in the NAcMed induces behaviour aversion. Collectively, our study reveals organizational and transcriptional differences in NAc subregions, and provides a framework for future dissection of NAc subregions in physiological and pathological conditions.

2023-01-14 | GSE222274 | GEO

b-Catenin Mediates the Development of Behavioral Resilience [ChIP-Seq]

Project description:Here we show that ?-catenin mediates pro-resilient and anxiolytic effects in mice in the nucleus accumbens (NAc), a key brain reward region, an effect that is mediated by ?-catenin signaling in D2-type medium spiny neurons (MSNs) specifically. Conversely, blocking ?-catenin function in NAc promotes susceptibility to chronic stress, and we show evidence of robust suppression of ?-catenin transcriptional activity in the NAc both of depressed humans examined postmortem as well as of mice that display a susceptible phenotype after chronic stress, with a converse upregulation in mice that are stress resilient. Using ChIP-seq, we demonstrate a global, genome-wide enrichment of ?-catenin in the NAc of resilient mice, and specifically identify Dicer1—important in small RNA (e.g., microRNA [miRNA]) biogenesis—as a critical ?-catenin target gene involved in mediating a resilient phenotype. Small RNA-seq after excising ?-catenin from the NAc in the context of chronic stress reveals dynamic ?-catenin-dependent miRNA regulation associated with resilience. Control: 2 samples, Resilient: 2 samples, Susceptible: 2 samples; DNA input: 1 sample.

2014-11-13 | E-GEOD-61294 | biostudies-arrayexpress

b-Catenin Mediates the Development of Behavioral Resilience [smallRNA-Seq]

Project description:Here we show that ?-catenin mediates pro-resilient and anxiolytic effects in mice in the nucleus accumbens (NAc), a key brain reward region, an effect that is mediated by ?-catenin signaling in D2-type medium spiny neurons (MSNs) specifically. Conversely, blocking ?-catenin function in NAc promotes susceptibility to chronic stress, and we show evidence of robust suppression of ?-catenin transcriptional activity in the NAc both of depressed humans examined postmortem as well as of mice that display a susceptible phenotype after chronic stress, with a converse upregulation in mice that are stress resilient. Using ChIP-seq, we demonstrate a global, genome-wide enrichment of ?-catenin in the NAc of resilient mice, and specifically identify Dicer1—important in small RNA (e.g., microRNA [miRNA]) biogenesis—as a critical ?-catenin target gene involved in mediating a resilient phenotype. Small RNA-seq after excising ?-catenin from the NAc in the context of chronic stress reveals dynamic ?-catenin-dependent miRNA regulation associated with resilience. GFP_Control: 12 samples, GFP_Resilient: 12 samples, GFP_Susceptible: 4 samples; CRE_Control: 12 samples, CRE_Susceptible: 8 samples.

2014-11-13 | E-GEOD-61295 | biostudies-arrayexpress

Effects of chronic morphine exposure on the transcriptome of nucleus accumbens (NAc) in mice

Project description:Morphine addiction causes major medical and social problems worldwide. Chronic morphine exposure results in the development of behavioral sensitization, accompanied by the disruption of brain homeostasis. As a key brain reward region, nucleus accumbens (NAc) plays a central role in brain reward mechanisms. However, the contribution of morphine exposure to NAc is poorly understood. Here we indicated that chronic morphine exposure induced neuroinflammation, abnormal neuronal physiology, and dysregulation of glycolytic metabolism in NAc. In summary, our findings illustrate the effects of morphine in NAc, and provide a new insight for development of future morphine addiction therapeutics.

2023-07-28 | GSE239387 | GEO

BAZ1B in Nucleus Accumbens Regulates Reward-Related Behaviors in Response to Distinct Emotional Stimuli

Project description:ATP-dependent chromatin remodeling proteins are being implicated increasingly in the regulation of complex behaviors, including models of several psychiatric disorders. Here, we demonstrate that Baz1b, an accessory subunit of the ISWI family of chromatin remodeling complexes, is upregulated in the nucleus accumbens (NAc), a key brain reward region, in both chronic cocaine-treated mice and mice that are resilient to chronic social defeat stress. In contrast, no regulation is seen in mice that are susceptible to this chronic stress. Viral-mediated overexpression of Baz1b, along with its associated subunit Smarca5, in mouse NAc is sufficient to potentiate both rewarding responses to cocaine, including cocaine self-administration, and resilience to chronic social defeat stress. However, despite these similar, proreward behavioral effects, genome-wide mapping of BAZ1B in NAc revealed mostly distinct subsets of genes regulated by these chromatin remodeling proteins after chronic exposure to either cocaine or social stress. Together, these findings suggest important roles for BAZ1B and its associated chromatin remodeling complexes in NAc in the regulation of reward behaviors to distinct emotional stimuli and highlight the stimulus-specific nature of the actions of these regulatory proteins. BAZ1B (WSTF) ChIP-seq of mouse. Cocaine vs Saline, 3 biological replicates. In social defeat model: Normal control vs Susceptible vs Resilient, 3 biological replicates.

2016-07-30 | E-GEOD-85005 | biostudies-arrayexpress

b-Catenin Mediates the Development of Behavioral Resilience [smallRNA-Seq]

Project description:Here we show that β-catenin mediates pro-resilient and anxiolytic effects in mice in the nucleus accumbens (NAc), a key brain reward region, an effect that is mediated by β-catenin signaling in D2-type medium spiny neurons (MSNs) specifically. Conversely, blocking β-catenin function in NAc promotes susceptibility to chronic stress, and we show evidence of robust suppression of β-catenin transcriptional activity in the NAc both of depressed humans examined postmortem as well as of mice that display a susceptible phenotype after chronic stress, with a converse upregulation in mice that are stress resilient. Using ChIP-seq, we demonstrate a global, genome-wide enrichment of β-catenin in the NAc of resilient mice, and specifically identify Dicer1—important in small RNA (e.g., microRNA [miRNA]) biogenesis—as a critical β-catenin target gene involved in mediating a resilient phenotype. Small RNA-seq after excising β-catenin from the NAc in the context of chronic stress reveals dynamic β-catenin-dependent miRNA regulation associated with resilience.

2014-11-13 | GSE61295 | GEO

b-Catenin Mediates the Development of Behavioral Resilience [ChIP-Seq]

2014-11-13 | GSE61294 | GEO

The circadian gene Nr1d1 in the mouse nucleus accumbens modulates social reward and anxiety-related behavior

Project description:Nuclear receptor subfamily 1, group D, member 1 (Nr1d1) (also known as Rev-erb alpha) has been linked to circadian rhythm regulation, mood-related behavior, and disorders associated with social deficits. Recent work from our laboratory found striking decreases in Nr1d1 in nucleus accumbens (NAc) in the maternal condition and indirect evidence that Nr1d1 was interacting with numerous addiction and reward-related genes to modulate social reward. In this study, we applied our insights from the maternal state to non-parental adult mice to determine whether decreases in Nr1d1 expression in NAc via adeno-associated viral (AAV) vectors and short hairpin RNA (shRNA)-mediated gene knockdown were sufficient to modulate social reward and mood-related behaviors. We also used microarray analysis of to identify gene expression alterations induced by the lowering of Nr1d1 expression. We used microarrays to evalute the effects of knockdown of mRNA for Nr1d1 in nuclues accumbens on gene expression.

2018-09-01 | GSE110363 | GEO

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