bioRxiv Science⌕ Search

bioRxiv · 10.64898/2026.04.03.716401

Alpha oscillations in the temporoparietal junction causally shift feedback-based social learning computations in strategic negotiation

Abstract

Human interactions span a range of contexts, from cooperation to competition. Negotiation, in particular, is a complex and extended social process in which individuals must reach mutually acceptable decisions despite conflicting incentives. The neural computations that support strategic behavior in such social dilemmas remain insufficiently understood. Here, we combine cognitive computational modeling, electroencephalography (EEG), functional Magnetic Resonance Imaging (fMRI), and fMRI-guided Transcranial Magnetic Stimulation (TMS) to demonstrate that oscillatory activity anchored in the temporoparietal junction (TPJ) causally shifts social learning during strategic bargaining. We found that TPJ metabolic activity and alpha-band oscillations are associated with the use of a feedback-based learning strategy during bargaining. Causal perturbation with rhythmic alpha-frequency TMS selectively modulates this strategy, increasing endogenous alpha oscillations and shifting behavioral learning parameters. Together, these findings reveal a frequency-specific mechanism within the neural substrates of social cognition that implements adaptive social learning, offering insights into potential neuromodulatory targets for ameliorating social dysfunction in neuropsychiatric conditions. Significance StatementStrategic negotiation requires predicting how others will respond to our actions, yet the neural computations supporting this form of social learning have remained elusive. By integrating computational modeling with EEG, fMRI, and frequency-specific TMS, we identify a mechanistic link between alpha-band activity in the temporoparietal junction (TPJ) and feedback-based learning during social exchange. Trial-by-trial estimates of this learning strategy were tracked by TPJ metabolic and oscillatory signals, and rhythmic alpha TMS causally enhanced both the neural signature and the behavioral expression of this strategy. These findings provide causal evidence for a frequency-specific mechanism within the neural systems that supports adaptive social learning. They also highlight the TPJ-alpha system as a promising target for neuromodulatory interventions to improve social functioning in neuropsychiatric conditions. Key FindingsO_LIModel-based behavioral analyses revealed two distinct strategies during social negotiation: a feedback-based learning mechanism (U-strategy) and a reputation-based updating mechanism (A-strategy). C_LIO_LIBoth strategies robustly predicted participants adaptive behavior across samples and conditions, and their modulation accounted for differences in negotiation outcomes. C_LIO_LIEEG analyses revealed frequency-specific alpha and beta power modulation linked to U-strategy computations during partner anticipation, localized to right temporoparietal regions. C_LIO_LIfMRI analyses revealed that trial-by-trial U-strategy estimates selectively modulated BOLD activity within the temporoparietal network associated with mentalizing. C_LIO_LIRhythmic alpha-frequency TMS over individually localized Theory-of-Mind TPJ sites causally altered negotiation behavior, shifting U-learning parameters toward a more conservative strategy. C_LIO_LITMS-EEG analyses demonstrated that alpha-frequency TMS induced time-locked alpha activity in functionally connected frontal sites, consistent with enhanced anticipatory computations. C_LIO_LITogether, these multimodal findings establish a causal, frequency-specific mechanism in the TPJ that implements social value learning during strategic bargaining. C_LI

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

Figueroa-Vargas, A., Valdebenito-Oyarzo, G., Martinez-Molina, M. P., Soto-Icaza, P., Figueroa-Taiba, P., Diaz-Diaz, M., Iriarte-Carter, M., Salinas, C., Stecher, X., Manterola, C., Zamorano, F., Valero-Cabre, A., Polania, R., Billeke, P.. 2026-04-05. Alpha oscillations in the temporoparietal junction causally shift feedback-based social learning computations in strategic negotiation. https://doi.org/10.64898/2026.04.03.716401

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related preprints

Different hippocampal subfield volumes predict source memory performance and general cognitive ability in an adult lifespan sample

Modest positive associations between episodic memory performance and whole hippocampal and hippocampal subfield volumes have been reported in numerous prior studies. A smaller number of studies have reported associations between hippocampal volume and performance on tests of non-mnemonic cognition. The present study examined whether these associations were evident in a lifespan sample of cognitively healthy adults. Of particular interest was whether any identified associations were sensitive to age, and whether associations between subfield volumes and mnemonic and non-mnemonic performance were subfield dependent. We acquired high-resolution T1- and T2-weighted structural images from 163 adults (18-87 years of age). Participants also undertook a comprehensive neuropsychological test battery and an in-scanner test of source memory. Principal components analysis was employed to reduce the neuropsychological test scores to 5 cognitive components. Two components reflected memory performance while the other three reflected different aspects of non-mnemonic cognition. Hippocampal subfields (Cornu Ammonis (CA)1, CA2-3, dentate gyrus (DG) and subiculum) were segmented and measured with the Automated Segmentation of Hippocampus Subfields (ASHS) package. Source memory performance was selectively associated across participants with CA2-3 volume. By contrast, both mnemonic and non-mnemonic component scores derived from the test battery were associated exclusively with the volume of the DG. All associations were age-invariant. The findings indicate that different cognitive domains can be dissociated by virtue of their associations with different hippocampal subfields. Of importance, these associations appear to be life-long and hence are unlikely to reflect individual differences in age-related decline in structural integrity.

neuroscience↗

Cell type specific astrocytic feedback regulates excitation inhibition balance and cortical network dynamics

Astrocytes actively regulate synaptic transmission and neuronal excitability, yet their role in orchestrating macroscopic cortical network regimes and slow-wave oscillations remains an active area of reasearch. This study investigates how bidirectional neuron astrocyte interactions shape emergent population dynamics using a computational network model of excitatory and inhibitory neurons coupled to an astrocyte. The results identify astrocytic feedback topology, rather than astrocytic coupling strength alone, as a key determinant of emergent cortical network dynamics. By systematically dissecting pathway-specific connectivity, it has been shown that the neuronal population driving astrocytic activation and the neuronal population receiving gliotransmission jointly determine whether the network occupies asynchronous irregular (AI), synchronous irregular (SI), synchronous regular(SR), asynchronous regular(AR) or quiescent regimes.Directing gliotransmission selectively onto excitatory neurons consistently promotes population synchrony regardless of the population influencing astrocytic dynamics, whereas selective modulation of inhibitory interneurons induces network quiescence via strong suppression. Under dual-target gliotransmission, network synchrony is dictated by the population driving astrocytic dynamics: excitatory-only drive promotes synchrony, while combined or inhibitory-specific drive preserves asynchronous states. Furthermore, the model reveals that astrocytic signaling kinetics provide an additional temporal control mechanism that regulates the frequency and persistence of self sustained up states.

neuroscience↗

VCP inhibition prevents cone photoreceptor degeneration in the cpfl1 mouse model of achromatopsia

Achromatopsia (ACHM) is a rare autosomal recessive retinal disorder characterized by absent cone photoreceptor function from early life, leading to severe visual impairment. Mutations in genes involved in the cone phototransduction cascade frequently result in elevated cyclic guanosine monophosphate (cGMP) levels and activation of stress pathways, including endoplasmic reticulum (ER) stress and the unfolded protein response. Targeting common downstream mechanisms rather than individual mutations may provide a broadly applicable therapeutic strategy. Here, we investigated whether pharmacological inhibition of valosin-containing protein (VCP), a key regulator of ER and protein homeostasis, can prevent cone degeneration in the spontaneous cone photoreceptor function loss 1 (cpfl1) mouse model of ACHM. Organotypic culture of retinal explants from cpfl1 mice were treated with the selective VCP inhibitor ML240. Cone survival, cell death, opsin expression and localization were assessed by TUNEL assay, immunohistochemistry, and quantitative image analysis. ML240 treatment significantly increased cone density and improved cone opsin expression and trafficking to the outer segments (OSs) in cpfl1 explants compared to controls. Importantly, rhodopsin trafficking in rod photoreceptors was unaffected, indicating that VCP inhibition did not impair normal rod phototransduction. These findings demonstrate that VCP inhibition by ML240 effectively preserves cone photoreceptors and improves cone-specific functional markers in the cpfl1 model. Targeting VCP may represent a mutation-independent therapeutic strategy for preventing cone death in ACHM.

neuroscience↗