Eyolfson Eric, Suesser Kirsten R B, Henry Holly, Bonilla-Del Río Itziar, Grandes Pedro, Mychasiuk Richelle, Christie Brian R
Division of Medical Sciences and Institute for Aging and Lifelong Health, University of Victoria, Victoria, BC, Canada.
Department of Neurosciences, Faculty of Medicine and Nursing, University of the Basque Country, Leioa, Spain.
Neuroscientist. 2025 Apr;31(2):195-214. doi: 10.1177/10738584241275583. Epub 2024 Sep 24.
Deficits in learning and memory are some of the most commonly reported symptoms following a traumatic brain injury (TBI). We will examine whether the neural basis of these deficits stems from alterations to bidirectional synaptic plasticity within the hippocampus. Although the CA1 subregion of the hippocampus has been a focus of TBI research, the dentate gyrus should also be given attention as it exhibits a unique ability for adult neurogenesis, a process highly susceptible to TBI-induced damage. This review examines our current understanding of how TBI results in deficits in synaptic plasticity, as well as how TBI-induced changes in endocannabinoid (eCB) systems may drive these changes. Through the synthesis and amalgamation of existing data, we propose a possible mechanism for eCB-mediated recovery in synaptic plasticity deficits. This hypothesis is based on the plausible roles of CB1 receptors in regulating inhibitory tone, influencing astrocytes and microglia, and modulating glutamate release. Dysregulation of the eCBs may be responsible for deficits in synaptic plasticity and learning following TBI. Taken together, the existing evidence indicates eCBs may contribute to TBI manifestation, pathogenesis, and recovery, but it also suggests there may be a therapeutic role for the eCB system in TBI.
学习和记忆缺陷是创伤性脑损伤（TBI）后最常报告的一些症状。我们将研究这些缺陷的神经基础是否源于海马体内双向突触可塑性的改变。尽管海马体的CA1亚区一直是TBI研究的重点，但齿状回也应受到关注，因为它具有独特的成年神经发生能力，而这一过程极易受到TBI诱导损伤的影响。本综述探讨了我们目前对TBI如何导致突触可塑性缺陷的理解，以及TBI诱导的内源性大麻素（eCB）系统变化如何驱动这些改变。通过对现有数据的综合与整合，我们提出了一种eCB介导的突触可塑性缺陷恢复的可能机制。这一假设基于CB1受体在调节抑制性张力、影响星形胶质细胞和小胶质细胞以及调节谷氨酸释放方面的合理作用。eCB的失调可能是TBI后突触可塑性和学习缺陷的原因。综上所述，现有证据表明eCB可能与TBI的表现、发病机制和恢复有关，但也表明eCB系统在TBI中可能具有治疗作用。
