Fredholm B B
Department of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden.
Pharmacol Toxicol. 1995 Feb;76(2):93-101. doi: 10.1111/j.1600-0773.1995.tb00111.x.
Of the known biochemical actions of caffeine, only inhibition of adenosine receptors occurs at concentrations achieved during normal human consumption of the drug. Under normal physiological conditions, adenosine is present in sufficient concentrations to activate A1 and A2a receptors. Via actions on A1 receptors, adenosine decreases neuronal firing and the release of neurotransmitters. The exact mechanisms are not known, but several possibilities are discussed. Via actions on A2a receptors, adenosine--and hence caffeine--can influence dopaminergic neurotransmission. Caffeine can induce rapid changes in gene expression and, somewhat later, marked adaptive changes. These include antiepileptic and neuroprotective changes. Thus, caffeine has a number of central effects directly or indirectly related to adenosine receptors. Some of these are potentially useful, and drug development based on the actions of caffeine should be interesting.
在咖啡因已知的生化作用中，只有在人类正常摄入该药物时所达到的浓度下才会发生对腺苷受体的抑制作用。在正常生理条件下，腺苷以足够的浓度存在以激活A1和A2a受体。通过作用于A1受体，腺苷会减少神经元放电和神经递质的释放。确切机制尚不清楚，但有几种可能性被讨论。通过作用于A2a受体，腺苷——以及咖啡因——可以影响多巴胺能神经传递。咖啡因可以诱导基因表达的快速变化，并且在稍晚些时候，会出现明显的适应性变化。这些变化包括抗癫痫和神经保护作用。因此，咖啡因具有许多与腺苷受体直接或间接相关的中枢效应。其中一些可能是有用的，基于咖啡因作用的药物开发应该会很有意思。
