School of Medical Science, Griffith University QLD, Australia ; Menzies Health Institute of Queensland, Griffith University QLD, Australia.
Department of Biological Sciences, Centre for the Neurobiology of Stress, University of Toronto Scarborough Toronto, ON, Canada.
Front Cell Neurosci. 2015 Mar 12;9:68. doi: 10.3389/fncel.2015.00068. eCollection 2015.
Heat shock response and homeostatic plasticity are mechanisms that afford functional stability to cells in the face of stress. Each mechanism has been investigated independently, but the link between the two has not been extensively explored. We explore this link. The heat shock response enables cells to adapt to stresses such as high temperature, metabolic stress and reduced oxygen levels. This mechanism results from the production of heat shock proteins (HSPs) which maintain normal cellular functions by counteracting the misfolding of cellular proteins. Homeostatic plasticity enables neurons and their target cells to maintain their activity levels around their respective set points in the face of stress or disturbances. This mechanism results from the recruitment of adaptations at synaptic inputs, or at voltage-gated ion channels. In this perspective, we argue that heat shock triggers homeostatic plasticity through the production of HSPs. We also suggest that homeostatic plasticity is a form of neuroprotection.
热休克反应和体内平衡可塑性是使细胞在面对压力时保持功能稳定的机制。这两个机制都已经被独立研究过，但它们之间的联系还没有被广泛探索。我们探讨了这一联系。热休克反应使细胞能够适应高温、代谢应激和低氧水平等压力。该机制源于热休克蛋白（HSPs）的产生，它通过对抗细胞蛋白的错误折叠来维持正常的细胞功能。体内平衡可塑性使神经元及其靶细胞能够在面对压力或干扰时维持其各自设定点的活动水平。这种机制源于在突触输入或电压门控离子通道处募集适应性。在这个角度上，我们认为热休克通过 HSP 的产生引发了体内平衡可塑性。我们还认为体内平衡可塑性是一种神经保护形式。
