慢性疼痛、记忆和损伤:来自蜗牛和大鼠伤害感受器的进化线索

E. Walters
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引用次数: 3

摘要

慢性疼痛的感觉成分可以进行比较研究和进化解释。疼痛通常是由痛觉感受器的激活引起的,痛觉感受器探测到有害的刺激。一项对大鼠和海蜗牛(Aplysia)的比较表明,两组的伤害感受器满足相同的功能定义,并表现出类似的功能改变,包括持续的高兴奋性和有害刺激后的突触增强。这些变化也与传统的学习和记忆有关。由于这些谱系的古老分化,一些相似之处可能反映了独立的进化。然而,到目前为止,与已知的长期神经元可塑性形式相关的分子信号代表了在所有后生动物细胞中发现的同源过程。目前用于慢性疼痛和记忆的持续可塑性机制可能最初是在最早的神经元中通过选择性招募核心细胞信号传导和效应系统来进化的,这些系统用于神经元修复、感觉补偿和与外周损伤相关的保护功能。
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Chronic Pain, Memory, and Injury: Evolutionary Clues from Snail and Rat Nociceptors
The sensory component of chronic pain is amenable to comparative study and evolutionaryinterpretations. Pain is usually initiated by activation of nociceptors, which detect damaging stimuli.A comparison of rats and a marine snail, Aplysia, shows that nociceptors in each group satisfy thesame functional definition and exhibit similar functional alterations, including persistenthyperexcitability and synaptic potentiation following noxious stimulation. These alterations are alsoassociated with conventional learning and memory. Because of the ancient divergence of theselineages, some similarities probably reflect independent evolution. However, the molecular signalslinked thus far to known forms of long-term neuronal plasticity represent homologous processes thatare found in all metazoan cells. Persistent plasticity mechanisms now used for chronic pain andmemory may have evolved originally in the earliest neurons by selective recruitment of core cellsignaling and effector systems for neuronal repair, sensory compensation, and protective functionsrelated to peripheral injury.
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