Memudu Adejoke Elizabeth, Olukade Baliqis Adejoke, Nwanama Kenechukwu Emmanuel, Alex Gideon S
Anatomy Department, Neuroscience Unit, Faculty of Basic Medical Sciences Edo State University Uzairue, Iyamho-Uzairue, Edo State, Nigeria.
Department of Molecular Medicine, Morsani College of Medicine, University of South Florida, Tampa, FL, United States.
Prog Brain Res. 2025;291:339-361. doi: 10.1016/bs.pbr.2025.01.018. Epub 2025 Feb 17.
There is an integral relationship between stress, brain function and behavior. Over the year's extensive research has led to the development of various models to explain the intricate intersection between brain and stress. This chapter delves into some of the theoretical frameworks that explains the neurobiological and behavioral responses to stress using key models of stress such as the allostatic load model, which is the most common model that describes how chronic stress affect brain structure and function resulting in long-term changes in regions such as the hippocampus, amygdala, and prefrontal cortex which phenotypically express as cognitive impairments, emotional dysfunction seen in various forms of neurological disorder. The neuro-endocrine model, follows the glucocorticoid cascade hypothesis, that associates prolonged stress exposure to hippocampal damage and cognitive decline via alteration in the hypothalamic-pituitary-adrenal (HPA) axis and the overproduction of stress hormones like cortisol which can induce hippocampal atrophy, impair learning and memory, and promote depressive-like behaviors. The neurobiological stress model addresses the role of the hypothalamic-pituitary-adrenal (HPA) axis and stress-related neurotransmitters in shaping behavioral responses, emphasizing alterations in neuroplasticity and synaptic function. These models demonstrate how chronic stress can alter neural plasticity, neurotransmitter systems, and synaptic connectivity, affecting behavior and cognitive function. Hence by integrating molecular, neurobiological, and behavioral perspectives, these models offer a comprehensive understanding of how stress alters brain activity and behavior. The chapter further showcase how these models direct the development of medical interventions, shedding light on potential therapies that target the underlying molecular mechanisms of stress-induced brain changes.
压力、脑功能和行为之间存在着一种内在联系。多年来，广泛的研究催生了各种模型，以解释大脑与压力之间复杂的交叉关系。本章深入探讨了一些理论框架，这些框架使用诸如应激负荷模型等关键压力模型来解释对压力的神经生物学和行为反应。应激负荷模型是最常见的模型，它描述了慢性压力如何影响脑结构和功能，导致海马体、杏仁核和前额叶皮质等区域发生长期变化，这些变化在表型上表现为认知障碍、在各种神经疾病中出现的情绪功能障碍。神经内分泌模型遵循糖皮质激素级联假说，该假说将长期暴露于压力与海马体损伤和认知衰退联系起来，其途径是下丘脑 - 垂体 - 肾上腺（HPA）轴的改变以及皮质醇等应激激素的过度产生，这些激素可导致海马体萎缩、损害学习和记忆，并促进类似抑郁的行为。神经生物学应激模型探讨了下丘脑 - 垂体 - 肾上腺（HPA）轴和与压力相关的神经递质在塑造行为反应中的作用，强调神经可塑性和突触功能的改变。这些模型展示了慢性压力如何改变神经可塑性、神经递质系统和突触连接性，从而影响行为和认知功能。因此，通过整合分子、神经生物学和行为学观点，这些模型提供了对压力如何改变大脑活动和行为的全面理解。本章还进一步展示了这些模型如何指导医学干预措施的开发，揭示了针对压力诱导的大脑变化的潜在分子机制的潜在疗法。
