IFB Adiposity Diseases, Leipzig University Medical Center, Germany.
Department of Neurology, Max Planck Institute for Human Cognitive and Brain Sciences Leipzig, Germany.
PLoS Comput Biol. 2020 Nov 30;16(11):e1008410. doi: 10.1371/journal.pcbi.1008410. eCollection 2020 Nov.
Computational modeling of dopamine transmission is challenged by complex underlying mechanisms. Here we present a new computational model that (I) simultaneously regards release, diffusion and uptake of dopamine, (II) considers multiple terminal release events and (III) comprises both synaptic and volume transmission by incorporating the geometry of the synaptic cleft. We were able to validate our model in that it simulates concentration values comparable to physiological values observed in empirical studies. Further, although synaptic dopamine diffuses into extra-synaptic space, our model reflects a very localized signal occurring on the synaptic level, i.e. synaptic dopamine release is negligibly recognized by neighboring synapses. Moreover, increasing evidence suggests that cognitive performance can be predicted by signal variability of neuroimaging data (e.g. BOLD). Signal variability in target areas of dopaminergic neurons (striatum, cortex) may arise from dopamine concentration variability. On that account we compared spatio-temporal variability in a simulation mimicking normal dopamine transmission in striatum to scenarios of enhanced dopamine release and dopamine uptake inhibition. We found different variability characteristics between the three settings, which may in part account for differences in empirical observations. From a clinical perspective, differences in striatal dopaminergic signaling contribute to differential learning and reward processing, with relevant implications for addictive- and compulsive-like behavior. Specifically, dopaminergic tone is assumed to impact on phasic dopamine and hence on the integration of reward-related signals. However, in humans DA tone is classically assessed using PET, which is an indirect measure of endogenous DA availability and suffers from temporal and spatial resolution issues. We discuss how this can lead to discrepancies with observations from other methods such as microdialysis and show how computational modeling can help to refine our understanding of DA transmission.
多巴胺传递的计算建模受到复杂的潜在机制的挑战。在这里,我们提出了一个新的计算模型,(I)同时考虑多巴胺的释放、扩散和摄取,(II)考虑多个末端释放事件,(III)通过纳入突触间隙的几何形状来包含突触和容积传递。我们能够验证我们的模型,因为它模拟的浓度值与经验研究中观察到的生理值相当。此外,尽管突触多巴胺扩散到突触外空间,但我们的模型反映了在突触水平上发生的非常局部的信号,即突触多巴胺释放几乎不会被相邻的突触识别。此外,越来越多的证据表明,认知表现可以通过神经影像学数据(例如 BOLD)的信号变异性来预测。多巴胺能神经元(纹状体、皮层)的靶区的信号变异性可能源于多巴胺浓度变异性。因此,我们比较了模拟正常多巴胺传递的纹状体中的模拟中的时空变异性与增强多巴胺释放和多巴胺摄取抑制的情景。我们发现三种情况下的变异性特征不同,这可能部分解释了经验观察的差异。从临床角度来看,纹状体多巴胺能信号传递的差异导致了不同的学习和奖励处理,这对成瘾和强迫样行为具有重要影响。具体来说,多巴胺能音调被认为会影响相位多巴胺,从而影响奖励相关信号的整合。然而,在人类中,DA 音调通常使用 PET 进行评估,这是内源性 DA 可用性的间接测量方法,并且存在时间和空间分辨率问题。我们讨论了这如何导致与微透析等其他方法的观察结果产生差异,并展示了计算建模如何帮助我们更好地理解 DA 传递。