scholarly journals Basolateral and central amygdala orchestrate how we learn whom to trust

2021 ◽  
Vol 4 (1) ◽  
Author(s):  
Ronald Sladky ◽  
Federica Riva ◽  
Lisa Anna Rosenberger ◽  
Jack van Honk ◽  
Claus Lamm
Keyword(s):  
Nucleus Accumbens ◽  
Choice Behavior ◽  
Basolateral Amygdala ◽  
Outcome Evaluation ◽  
Reward Processing ◽  
Trust Game ◽  
Central Amygdala ◽  
Learning Success ◽  
Fmri Study ◽  
Human Neuroimaging

AbstractCooperation and mutual trust are essential in our society, yet not everybody is trustworthy. In this fMRI study, 62 healthy volunteers performed a repeated trust game, placing trust in a trustworthy or an untrustworthy player. We found that the central amygdala was active during trust behavior planning while the basolateral amygdala was active during outcome evaluation. When planning the trust behavior, central and basolateral amygdala activation was stronger for the untrustworthy player compared to the trustworthy player but only in participants who actually learned to differentiate the trustworthiness of the players. Independent of learning success, nucleus accumbens encoded whether trust was reciprocated. This suggests that learning whom to trust is not related to reward processing in the nucleus accumbens, but rather to engagement of the amygdala. Our study overcomes major empirical gaps between animal models and human neuroimaging and shows how different subnuclei of the amygdala and connected areas orchestrate learning to form different subjective trustworthiness beliefs about others and guide trust choice behavior.

scholarly journals In amygdala we trust: different contributions of the basolateral and central amygdala in learning whom to trust

2021 ◽  
Author(s):  
Ronald Sladky ◽  
Federica Riva ◽  
Lisa Rosenberger ◽  
Jack van Honk ◽  
Claus Lamm
Keyword(s):  
Basolateral Amygdala ◽  
Human Subjects ◽  
Brain Structures ◽  
Trust Game ◽  
Rodent Models ◽  
Mutual Trust ◽  
Central Amygdala ◽  
Interaction Partners ◽  
Improved Learning

Human societies are built on cooperation and mutual trust, but not everybody is trustworthy. Research on rodents suggests an essential role of the basolateral amygdala (BLA) in learning from social experiences (Hernandez-Lallement J et al., 2016), which was also confirmed in human subjects with selective bilateral BLA damage as they failed to adapt their trust behavior towards trustworthy vs. untrustworthy interaction partners (Rosenberger LA et al., 2019). However, neuroimaging in neurotypical populations did not consistently report involvement of the amygdala in trust behavior. This might be explained by the difficulty of differentiating between amygdala's structurally and functionally different subnuclei, i.e., the BLA and central amygdala (CeA), which have even antagonistic features particularly in trust behavior (van Honk J et al., 2013). Here, we used fMRI of the amygdala subnuclei of neurotypical adults (n=31f/31m) engaging in the repeated trust game. Our data show that both the BLA and the CeA play a role and indeed differentially: While the BLA was most active when obtaining feedback on whether invested trust had been reciprocated or not, the CeA was most active when subjects were preparing their next trust decision. In the latter phase, improved learning was associated with higher activation differences in response to untrustworthy vs. trustworthy trustees, in both BLA and CeA. Our data not only translate to rodent models and support our earlier findings in BLA-damaged subjects, but also show the specific contributions of other brain structures in the amygdala-centered network in learning whom to trust, and better not to trust.

The Decision-making and Outcome Evaluation during a Repeated Trust Game

2015 ◽  
Vol 47 (8) ◽  
pp. 1028 ◽  
Author(s):  
Yiwen WANG ◽  
Zhen ZHANG ◽  
Sheng YUAN ◽  
Fengbo GUO ◽  
Shaoying HE ◽  
...  
Keyword(s):  
Decision Making ◽  
Outcome Evaluation ◽  
Trust Game

Dopaminylation in Psychostimulant use Disorder Protects Against Psychostimulant Seeking Behavior by Normalizing Nucleus Accumbens (NAc) Dopamine Expression

2021 ◽  
Vol 09 ◽  
Author(s):  
Kenneth Blum ◽  
Mark S Gold ◽  
Jean L. Cadet ◽  
David Baron ◽  
Abdalla Bowirrat ◽  
...  
Keyword(s):  
Nucleus Accumbens ◽  
Histone H3 ◽  
D2 Receptor ◽  
Reward Processing ◽  
Allelic Polymorphism ◽  
Cocaine Withdrawal ◽  
Src Signaling ◽  
Chronic Cocaine ◽  
Cocaine Seeking ◽  
Seeking Behavior

Background: Repeated cocaine administration changes histone acetylation and methylation on Lys residues and Deoxyribonucleic acid (DNA) within the nucleus accumbens (NAc). Recently Nestler’s group explored histone Arg (R) methylation in reward processing models. Damez-Werno et al. (2016) reported that during investigator and selfadministration experiments, the histone mark protein-R-methyltransferase-6 (PRMT6) and asymmetric dimethylation of R2 on histone H3 (H3R2me2a) decreased in the rodent and cocaine-dependent human NAc. Overexpression of PRMT6 in D2-MSNs in all NAc neurons increased cocaine seeking, whereas PRMT6 overexpression in D1-MSNs protects against cocaine-seeking. Hypothesis: Hypothesizing that dopaminylation (H3R2me2a binding) occurs in psychostimulant use disorder (PSU), and the binding inhibitor Srcin1, like the major DRD2 A2 allelic polymorphism, protects against psychostimulant seeking behavior by normalizing nucleus accumbens (NAc) dopamine expression. Discussion: Numerous publications confirmed the association between the DRD2 Taq A1 allele (30-40 lower D2 receptor numbers) and severe cocaine dependence. Lepack et al. (2020) found that acute cocaine increases dopamine in NAc synapses, results in histone H3 glutamine 5 dopaminylation (H3Q5dop), and consequent inhibition of D2 expression. The inhibition increases with chronic cocaine use and accompanies cocaine withdrawal. They also found that the Src kinase sig-naling inhibitor 1 (Srcin1 or p140CAP) during cocaine withdrawal reduced H3R2me2a binding. Consequently, this inhibited dopaminylation induced a “homeostatic brake.” Conclusion: The decrease in Src signaling in NAc D2-MSNs, like the DRD2 Taq A2 allele, a well-known genetic mechanism protective against SUD normalized nucleus accumbens (NAc) dopamine expression and decreased cocaine reward and motivation to self-administer cocaine. The Srcin1 may be an important therapeutic target.

Opposing Influence of Basolateral Amygdala and Footshock Stimulation on Neurons of the Central Amygdala

2006 ◽  
Vol 59 (9) ◽  
pp. 801-811 ◽  
Author(s):  
J. Amiel Rosenkranz ◽  
Deanne M. Buffalari ◽  
Anthony A. Grace
Keyword(s):  
Basolateral Amygdala ◽  
Central Amygdala

scholarly journals Dopamine D1and NMDA Receptors Mediate Potentiation of Basolateral Amygdala-Evoked Firing of Nucleus Accumbens Neurons

2001 ◽  
Vol 21 (16) ◽  
pp. 6370-6376 ◽  
Author(s):  
Stan B. Floresco ◽  
Charles D. Blaha ◽  
Charles R. Yang ◽  
Anthony G. Phillips
Keyword(s):  
Nucleus Accumbens ◽  
Nmda Receptors ◽  
Basolateral Amygdala

scholarly journals Timing of Impulses From the Central Amygdala and Bed Nucleus of the Stria Terminalis to the Brain Stem

2008 ◽  
Vol 100 (6) ◽  
pp. 3429-3436 ◽  
Author(s):  
Frank Z. Nagy ◽  
Denis Paré
Keyword(s):  
Brain Stem ◽  
Basolateral Amygdala ◽  
Stria Terminalis ◽  
Central Amygdala ◽  
Response Latencies ◽  
Bed Nucleus ◽  
Antidromic Responses ◽  
The Brain ◽  
Antidromic Response ◽  
Shed Light

The amygdala and bed nucleus of the stria terminalis (BNST) are thought to subserve distinct functions, with the former mediating rapid fear responses to discrete sensory cues and the latter longer “anxiety-like” states in response to diffuse environmental contingencies. However, these structures are reciprocally connected and their projection sites overlap extensively. To shed light on the significance of BNST–amygdala connections, we compared the antidromic response latencies of BNST and central amygdala (CE) neurons to brain stem stimulation. Whereas the frequency distribution of latencies was unimodal in BNST neurons (∼10-ms mode), that of CE neurons was bimodal (∼10- and ∼30-ms modes). However, after stria terminalis (ST) lesions, only short-latency antidromic responses were observed, suggesting that CE axons with long conduction times course through the ST. Compared with the direct route, the ST greatly lengthens the path of CE axons to the brain stem, an apparently disadvantageous arrangement. Because BNST and CE share major excitatory basolateral amygdala (BL) inputs, lengthening the path of CE axons might allow synchronization of BNST and CE impulses to brain stem when activated by BL. To test this, we applied electrical BL stimuli and compared orthodromic response latencies in CE and BNST neurons. The latency difference between CE and BNST neurons to BL stimuli approximated that seen between the antidromic responses of BNST cells and CE neurons with long conduction times. These results point to a hitherto unsuspected level of temporal coordination between the inputs and outputs of CE and BNST neurons, supporting the idea of shared functions.

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