Saransaari Pirjo, Oja Simo S
Tampere Brain Research Center, Medical School, University of Tampere, Finland.
Neurochem Res. 2002 Sep;27(9):911-8. doi: 10.1023/a:1020343631833.
Adenosine is a neuromodulator known to inhibit the synaptic release of neurotransmitters, e.g., glutamate, and to hyperpolarize postsynaptic neurons. The release of adenosine is markedly enhanced under ischemic conditions. It may then act as an endogenous neuroprotectant against cerebral ischemia and excitotoxic neuronal damage. The mechanisms by which adenosine is released from nervous tissue are not fully known, particularly in the immature brain. We now characterized the release of [3H]adenosine from hippocampal slices from developing (7-day-old) and adult (3-month-old) mice using a superfusion system. The properties of the release differed only partially in the immature and mature hippocampus. The K(+)-evoked release was Ca2+ and Na+ dependent. Anion channels were also involved. Ionotropic glutamate receptor agonists potentiated the release in a receptor-mediated manner. Activation of metabotropic glutamate receptors enhanced the release in developing mice, with group II receptors alone being effective. The evoked adenosine release apparently provides neuroprotective effects against excitotoxicity under cell-damaging conditions. Taurine had no effect on adenosine release in adult mice, but depressed the release concentration dependently in the immature hippocampus.
腺苷是一种神经调质，已知其可抑制神经递质（如谷氨酸）的突触释放，并使突触后神经元超极化。在缺血条件下，腺苷的释放会显著增强。然后它可能作为一种内源性神经保护剂，对抗脑缺血和兴奋性毒性神经元损伤。腺苷从神经组织释放的机制尚未完全明确，尤其是在未成熟脑内。我们现在使用灌流系统对发育中（7日龄）和成年（3月龄）小鼠海马切片中[3H]腺苷的释放进行了表征。未成熟和成熟海马中释放的特性仅部分不同。钾离子诱发的释放依赖于钙离子和钠离子，阴离子通道也参与其中。离子型谷氨酸受体激动剂以受体介导的方式增强释放。代谢型谷氨酸受体的激活在发育中小鼠中增强了释放，仅II组受体起作用。诱发的腺苷释放在细胞损伤条件下显然对兴奋性毒性具有神经保护作用。牛磺酸对成年小鼠的腺苷释放没有影响，但在未成熟海马中浓度依赖性地抑制释放。
