期刊
FRONTIERS IN BEHAVIORAL NEUROSCIENCE
卷 17, 期 -, 页码 -出版社
FRONTIERS MEDIA SA
DOI: 10.3389/fnbeh.2023.1060786
关键词
dopamine; intelligence; working memory; attention; receptor subtypes; behavioral genetics
Genetic evidence suggests that intelligence differences cannot be attributed to a single dominant cause. However, some variations may be linked to the balance of dopamine D1 and D2 receptors, which regulate executive functions like attention and working memory. Dual-state dopamine signaling may contribute to intelligence variation and can be influenced by experiences/training, although it may only explain a small portion of the total variance.
Genetic evidence strongly suggests that individual differences in intelligence will not be reducible to a single dominant cause. However, some of those variations/changes may be traced to tractable, cohesive mechanisms. One such mechanism may be the balance of dopamine D1 (D1R) and D2 (D2R) receptors, which regulate intrinsic currents and synaptic transmission in frontal cortical regions. Here, we review evidence from human, animal, and computational studies that suggest that this balance (in density, activity state, and/or availability) is critical to the implementation of executive functions such as attention and working memory, both of which are principal contributors to variations in intelligence. D1 receptors dominate neural responding during stable periods of short-term memory maintenance (requiring attentional focus), while D2 receptors play a more specific role during periods of instability such as changing environmental or memory states (requiring attentional disengagement). Here we bridge these observations with known properties of human intelligence. Starting from theories of intelligence that place executive functions (e.g., working memory and attentional control) at its center, we propose that dual-state dopamine signaling might be a causal contributor to at least some of the variation in intelligence across individuals and its change by experiences/training. Although it is unlikely that such a mechanism can account for more than a modest portion of the total variance in intelligence, our proposal is consistent with an array of available evidence and has a high degree of explanatory value. We suggest future directions and specific empirical tests that can further elucidate these relationships.
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