Neuroscience Program, University of Illinois at Urbana-Champaign, 505 S. Goodwin Ave., Urbana, IL 61801, USA.
Neurobiol Aging. 2010 Dec;31(12):2136-45. doi: 10.1016/j.neurobiolaging.2008.12.003. Epub 2009 Jan 28.
Increases in blood glucose levels are an important component of the mechanisms by which epinephrine enhances memory formation. The present experiments addressed the hypothesis that a dysfunction in the blood glucose response to circulating epinephrine contributes to age-related memory impairments. Doses of epinephrine and glucagon that significantly increased blood glucose levels in young adult rats were far less effective at doing so in 2-year-old rats. In young rats, epinephrine and glucose were about equally effective in enhancing memory and in prolonging post-training release of acetylcholine in the hippocampus. However, glucose was more effective than epinephrine in enhancing both memory and acetylcholine release in aged rats. These results suggest that an uncoupling between circulating epinephrine and glucose levels in old rats may lead to an age-related reduction in the provision of glucose to the brain during training. This in turn may contribute to age-related changes in memory and neural plasticity.
血糖水平的升高是肾上腺素增强记忆形成机制的重要组成部分。本实验提出了一个假设，即循环肾上腺素引起的血糖反应功能障碍导致与年龄相关的记忆损伤。在年轻成年大鼠中，肾上腺素和胰高血糖素的剂量显著升高血糖水平，但在 2 岁大鼠中效果要差得多。在年轻大鼠中，肾上腺素和葡萄糖在增强记忆和延长海马乙酰胆碱的训练后释放方面同样有效。然而，在老年大鼠中，葡萄糖比肾上腺素更有效地增强记忆和乙酰胆碱的释放。这些结果表明，老年大鼠中循环肾上腺素和血糖水平之间的解偶联可能导致在训练过程中大脑葡萄糖供应减少，从而导致与年龄相关的记忆和神经可塑性变化。
