Stone T W, Connick J H, Bartrup J T
Department of Pharmacology, University of Glasgow, Scotland, U.K.
Brain Res. 1990 Feb 5;508(2):333-6. doi: 10.1016/0006-8993(90)90419-c.
Perfusion of hippocampal slices with magnesium-free media elicits epileptiform activity attributable partly to the activity of N-methyl-D-aspartate (NMDA) receptors, but recent reports have documented an NMDA-independent enhancement of orthodromic potentials by moderate reductions in magnesium concentration. The present experiments indicate that this enhancement is comparable with that produced by perfusion with an adenosine antagonist, 8-phenyltheophylline, and that superfusion with this compound or adenosine deaminase precludes any enhancement of potential size in low magnesium solutions. The low magnesium enhancement is probably attributable to the recently described magnesium dependency of presynaptic inhibition by adenosine.
用无镁培养基灌注海马切片会引发癫痫样活动，部分归因于N-甲基-D-天冬氨酸（NMDA）受体的活性，但最近的报告记录了通过适度降低镁浓度可在不依赖NMDA的情况下增强顺向电位。目前的实验表明，这种增强与用腺苷拮抗剂8-苯基茶碱灌注所产生的增强相当，并且用该化合物或腺苷脱氨酶进行过灌注可防止在低镁溶液中电位大小的任何增强。低镁增强可能归因于最近描述的腺苷对突触前抑制的镁依赖性。
