Psarropoulou C, Kostopoulos G
Department of Physiology, University of Patras Medical School, Greece.
Epilepsia. 1993 Jan-Feb;34(1):24-32. doi: 10.1111/j.1528-1157.1993.tb02372.x.
Tottering mice are an experimental model of genetically determined generalized epilepsy of the absence type. We investigated possible mechanisms underlying epileptogenic hyperexcitability in these mice by studying input/output (I/O) curves of the extracellular response of CA1 neurons to stratum radiatum stimulation in hippocampal slices maintained in vitro. Increases in extracellular potassium are considered to contribute to epileptogenesis, whereas adenosine has been proposed to be an endogenous antiepileptic agent. Moderate elevations (+2 mM) of extracellular K+ concentrations induced a significantly smaller increase of this response (leftward shift of the input/output curves) in slices from epileptic mice as compared with controls. Perfusion of slices with adenosine 10 microM decreased excitability in both groups of slices, especially with regard to response threshold. Adenosine more effectively decreased the responses elicited by low-intensity stimulation than those elicited by high intensity. No significant difference between the groups of slices was observed. On the basis of the present data, it is unlikely that the previously observed hyperexcitability of hippocampal neurons of tottering mice results from a genetically altered sensitivity to moderate increases in [K+]o or to adenosine.
蹒跚小鼠是遗传性失神型全身性癫痫的实验模型。我们通过研究体外培养的海马切片中CA1神经元对辐射层刺激的细胞外反应的输入/输出（I/O）曲线，来探究这些小鼠癫痫源性过度兴奋的潜在机制。细胞外钾离子的增加被认为与癫痫发生有关，而腺苷被认为是一种内源性抗癫痫剂。与对照组相比，癫痫小鼠切片中细胞外K+浓度适度升高（+2 mM）引起的这种反应的增加明显较小（输入/输出曲线向左移动）。用10 microM腺苷灌注切片降低了两组切片的兴奋性，尤其是在反应阈值方面。腺苷对低强度刺激引起的反应的降低作用比对高强度刺激引起的反应更有效。两组切片之间未观察到显著差异。根据目前的数据，之前观察到的蹒跚小鼠海马神经元过度兴奋不太可能是由对[K+]o适度增加或腺苷的遗传敏感性改变所致。
