ArticlePLoS biology2025
Regulation of working memory switches from striatal dopamine D2-receptor to D1-receptor neurons under high cognitive load.
Article in PLoS biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
- Lateralized nigrostriatal dopamine pathway activation promotes early reversal learning.Frontiers in behavioral neuroscience · 2025Article
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15 authors.
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Abstract
Working memory (WM) is a fundamental cognitive function crucial adaptive behavior. The intricate interplay between the frontal cortex and striatum in governing WM maintenance and updating remains a central question. In this study, we employed optogenetics to demonstrate that inhibiting both dorsomedial striatum (DMS) D1R- and D2R-neurons enhances WM, while their activation impairs it across T-maze and operant-based delayed-non-match-to-place (DNMTP) paradigms in mice. Notably, these neurons selectively modulate WM maintenance and retrieval, with no impact on encoding. Analysis through signal detection theory (SDT) revealed specific regulation of WM signal detection sensitivity, with no alterations in motivational or motor states during the operant DNMTP task. Interestingly, DMS D2R-neurons govern WM regulation under low cognitive load, switching to D1R-neurons as cognitive load increases. Activation of DMS D1R-neurons during the delay phase severely impairs WM under high cognitive load, a deficit rescued by optogenetic inhibition of dopaminergic neurons in the ventral tegmental area (VTA) and substantia nigra pars compacta (SNc), or dopaminergic terminals in DMS. Additionally, treatment with the D1R antagonist SCH39166, but not the D2R antagonist Sulpiride mitigates these impairments. Collectively, our findings propose a "relay" model wherein cognitive load-dependent WM control switches from DMS D2R- to D1R-neurons, offering nuanced, complementary, and inhibitory regulation of WM maintenance and retrieval. This study suggests potential strategies to enhance WM by promoting a suppressive state in DMS and to increase WM capacity through specific modulation of DMS D1R-neurons.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.