ArticlePLoS computational biology2020
Signaling models for dopamine-dependent temporal contiguity in striatal synaptic plasticity.
Article in PLoS computational biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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14 citing papers in PubMed, 19 citations in OpenAlex.
- Discrete spatiotemporal encoding of striatal dopamine transmission.Science (New York, N.Y.) · 2025Article
- Novel impact of metal ion-induced cell death on diabetic cardiomyopathy pathogenesis and therapy.Apoptosis : an international journal on programmed cell death · 2025Review
- Editorial for This Special Issue "Synaptic Transmission: From Molecular to Neural Network Levels".Biomedicines · 2024Article
- Neuronal implementation of the temporal difference learning algorithm in the midbrain dopaminergic system.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Advances in understanding the function of alpha-synuclein: implications for Parkinson's disease.Brain : a journal of neurology · 2023Review
- Unraveling the mysteries of dendritic spine dynamics: Five key principles shaping memory and cognition.Proceedings of the Japan Academy. Series B, Physical and biological sciences · 2023Article
- Psychosis spectrum illnesses as disorders of prefrontal critical period plasticity.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2023Review
- Antidepressant-like effects of cinnamamide derivative M2 via DActa pharmacologica Sinica · 2022Article
- A proxy measure of striatal dopamine predicts individual differences in temporal precision.Psychonomic bulletin & review · 2022Article
- Green fluorescent cAMP indicator of high speed and specificity suitable for neuronal live-cell imaging.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- A behavioural correlate of the synaptic eligibility trace in the nucleus accumbens.Scientific reports · 2022Article
- Acute and chronic effects by nicotine on striatal neurotransmission and synaptic plasticity in the female rat brain.Frontiers in molecular neuroscience · 2022Article
- The critical balance between dopamine D2 receptor and RGS for the sensitive detection of a transient decay in dopamine signal.PLoS computational biology · 2021Article
- Spine dynamics in the brain, mental disorders and artificial neural networks.Nature reviews. Neuroscience · 2021Review
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Authors and funding
4 authors at 2 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
Animals remember temporal links between their actions and subsequent rewards. We previously discovered a synaptic mechanism underlying such reward learning in D1 receptor (D1R)-expressing spiny projection neurons (D1 SPN) of the striatum. Dopamine (DA) bursts promote dendritic spine enlargement in a time window of only a few seconds after paired pre- and post-synaptic spiking (pre-post pairing), which is termed as reinforcement plasticity (RP). The previous study has also identified underlying signaling pathways; however, it still remains unclear how the signaling dynamics results in RP. In the present study, we first developed a computational model of signaling dynamics of D1 SPNs. The D1 RP model successfully reproduced experimentally observed protein kinase A (PKA) activity, including its critical time window. In this model, adenylate cyclase type 1 (AC1) in the spines/thin dendrites played a pivotal role as a coincidence detector against pre-post pairing and DA burst. In particular, pre-post pairing (Ca2+ signal) stimulated AC1 with a delay, and the Ca2+-stimulated AC1 was activated by the DA burst for the asymmetric time window. Moreover, the smallness of the spines/thin dendrites is crucial to the short time window for the PKA activity. We then developed a RP model for D2 SPNs, which also predicted the critical time window for RP that depended on the timing of pre-post pairing and phasic DA dip. AC1 worked for the coincidence detector in the D2 RP model as well. We further simulated the signaling pathway leading to Ca2+/calmodulin-dependent protein kinase II (CaMKII) activation and clarified the role of the downstream molecules of AC1 as the integrators that turn transient input signals into persistent spine enlargement. Finally, we discuss how such timing windows guide animals' reward learning.
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