Department of Anatomy, Brain Health Research Centre, University of Otago, Dunedin 9054, New Zealand.
Department of Psychology, University of Sheffield, Sheffield, S10 2TP, UK.
Curr Neuropharmacol. 2024;22(9):1513-1527. doi: 10.2174/1570159X21666230801110359.
Regional changes in corticostriatal transmission induced by phasic dopaminergic signals are an essential feature of the neural network responsible for instrumental reinforcement during discovery of an action. However, the timing of signals that are thought to contribute to the induction of corticostriatal plasticity is difficult to reconcile within the framework of behavioural reinforcement learning, because the reinforcer is normally delayed relative to the selection and execution of causally-related actions.
While recent studies have started to address the relevance of delayed reinforcement signals and their impact on corticostriatal processing, our objective was to establish a model in which a sensory reinforcer triggers appropriately delayed reinforcement signals relayed to the striatum via intact neuronal pathways and to investigate the effects on corticostriatal plasticity.
We measured corticostriatal plasticity with electrophysiological recordings using a light flash as a natural sensory reinforcer, and pharmacological manipulations were applied in an anesthetized rat model preparation.
We demonstrate that the spiking of striatal neurons evoked by single-pulse stimulation of the motor cortex can be potentiated by a natural sensory reinforcer, operating through intact afferent pathways, with signal timing approximating that required for behavioural reinforcement. The pharmacological blockade of dopamine receptors attenuated the observed potentiation of corticostriatal neurotransmission.
This novel model of corticostriatal plasticity offers a behaviourally relevant framework to address the physiological, anatomical, cellular, and molecular bases of instrumental reinforcement learning.
由相位多巴胺信号诱导的皮质纹状体传递的区域变化是负责在发现动作期间对工具性强化的神经网络的重要特征。然而,被认为有助于诱导皮质纹状体可塑性的信号的时间难以与行为强化学习框架相协调,因为强化物通常相对于因果相关动作的选择和执行而延迟。
虽然最近的研究已经开始解决延迟强化信号的相关性及其对皮质纹状体处理的影响,但我们的目的是建立一个模型,其中感觉强化物通过完整的神经元途径触发适当延迟的强化信号传递到纹状体,并研究对皮质纹状体可塑性的影响。
我们使用光闪烁作为自然感觉强化物,通过电生理记录来测量皮质纹状体可塑性,并且在麻醉大鼠模型制备中应用药理学操作。
我们证明,通过完整的传入途径,通过单脉冲刺激运动皮层诱发的纹状体神经元的尖峰可以被自然感觉强化物增强,信号时间接近行为强化所需的时间。多巴胺受体的药理学阻断减弱了观察到的皮质纹状体神经传递的增强。
这种新的皮质纹状体可塑性模型提供了一个与行为相关的框架,用于解决工具性强化学习的生理、解剖、细胞和分子基础。