Addae J I, Stone T W
Department of Physiology, St. George's Hospital Medical School, London, U.K.
Electroencephalogr Clin Neurophysiol. 1988 Feb;69(2):186-9. doi: 10.1016/0013-4694(88)90214-3.
Adenosine and analogues, and antagonists to adenosine and putative excitatory amino acid transmitters were topically applied to the cerebral cortex of urethane-anaesthetised rats and their effects on the somatosensory evoked potentials (SEPs) examined. 2-Chloro-adenosine decreased the amplitude of the SEPs whereas adenosine did not. Both L-(-)N6-phenyl-isopropyladenosine (L-PIA) and 5'-N-ethylcarboxamide adenosine (NECA) depressed the SEPs; the effect of L-PIA was more marked than that of NECA. 8-p-Sulphophenyl theophylline increased the amplitude of the SEPs and also inhibited the effects of 2-chloro-adenosine and L-PIA. Kynurenic acid decreased the amplitude of the SEPs. The results suggest that the initial component of the SEP is a post-synaptic event and that endogenous adenosine probably modulates thalamo-cortical synaptic transmission.
将腺苷及其类似物，以及腺苷拮抗剂和假定的兴奋性氨基酸递质局部应用于氨基甲酸乙酯麻醉大鼠的大脑皮层，并检测它们对体感诱发电位（SEP）的影响。2-氯腺苷降低了SEP的振幅，而腺苷则没有。L-(-)N6-苯基异丙基腺苷（L-PIA）和5'-N-乙基甲酰胺腺苷（NECA）均使SEP降低；L-PIA的作用比NECA更显著。8-对磺基苯甲基黄嘌呤增加了SEP的振幅，并且还抑制了2-氯腺苷和L-PIA的作用。犬尿喹啉酸降低了SEP的振幅。结果表明，SEP的起始成分是突触后事件，内源性腺苷可能调节丘脑-皮层突触传递。
