Deckert J, Gleiter C H
Department of Psychiatry, University of Würzburg, Federal Republic of Germany.
J Neural Transm Suppl. 1994;43:23-31.
Adenosine is now widely accepted as the major inhibitory neuromodulator in the central nervous system besides GABA. It has been suggested to be an endogenous neuroprotective metabolite. In situations of metabolic stress, e.g. ischemia adenosine decreases energy demand and increases energy supply. Of particular relevance in this context is its modulation of glutamate release. A shift of this adenosine-glutamate balance in favor of adenosine helps to restore function at the cellular, organ and organism level. Adenosine A1 receptor agonists and metabolic inhibitors, e.g. of transport, deaminase and xanthine oxidase have been demonstrated to be effective in different animal models of ischemia. Nimodipine, a L-type channel calcium antagonist currently in clinical trials for stroke and dementia syndromes, has now been shown to be a potent adenosine transport inhibitor in clinically relevant concentrations. Increase of adenosinergic neuromodulation may well be one of several future therapeutic strategies in neuroprotection.
除γ-氨基丁酸（GABA）外，腺苷现在被广泛认为是中枢神经系统中的主要抑制性神经调质。它被认为是一种内源性神经保护代谢物。在代谢应激情况下，如缺血时，腺苷会降低能量需求并增加能量供应。在这种情况下，其对谷氨酸释放的调节尤为重要。这种腺苷 - 谷氨酸平衡向有利于腺苷的方向转变有助于在细胞、器官和机体水平恢复功能。腺苷A1受体激动剂和代谢抑制剂，如转运、脱氨酶和黄嘌呤氧化酶的抑制剂，已被证明在不同的缺血动物模型中有效。尼莫地平，一种目前正在进行中风和痴呆综合征临床试验的L型通道钙拮抗剂，现已证明在临床相关浓度下是一种有效的腺苷转运抑制剂。增强腺苷能神经调节很可能是未来神经保护的几种治疗策略之一。
