Basal amygdala-nucleus accumbens glutamate neurons respond to either social reward or social aversion
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA909332 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR22556436_1.fastq.gz | Fastqsanger.gz | |||
| SRR22556436_2.fastq.gz | Fastqsanger.gz | |||
| SRR22556437_1.fastq.gz | Fastqsanger.gz | |||
| SRR22556437_2.fastq.gz | Fastqsanger.gz | |||
| SRR22556438_1.fastq.gz | Fastqsanger.gz |
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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.
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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.
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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.
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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.
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Project description:Psychedelics are a broad class of drugs defined by their ability to induce an altered state of consciousness. These drugs have been used for millennia in both spiritual and medicinal contexts, and a number of recent clinical successes have spurred a renewed interest in developing psychedelic therapies. Nevertheless, a unifying mechanism that can account for these shared phenomenological and therapeutic properties remains unknown. Here we demonstrate in mice that the ability to reopen the social reward learning critical period is a shared property across psychedelics. Interestingly, the time course of critical period reopening is proportional to the duration of acute subjective effects reported in humans. Furthermore, the ability to reinstate social reward learning in adulthood is paralleled by metaplastic restoration of oxytocin mediated long-term depression (OT-LTD) in the Nucleus Accumbens (NAc). Finally, identification of differentially expressed genes in the ‘open state’ versus ‘closed state’, provides evidence that reorganization of the extracellular matrix (ECM) is a common downstream mechanism underlying psychedelic mediated critical period reopening. Together these results have significant implications for the implementation of psychedelics in clinical practice, as well as the design of novel compounds for the treatment of neuropsychiatric disease.
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