Fowler J C, Partridge L D, Gervitz L
Department of Physiology, Texas Tech University Health Sciences Center, Lubbock, TX 79430,
Brain Res. 1999 Jan 9;815(2):414-8. doi: 10.1016/s0006-8993(98)01114-7.
The nitric oxide donor hydroxylamine (NH2OH) induced a transient depression of the evoked synaptic potential recorded in the rat hippocampal CA1 region. This depression was abolished with an adenosine A1 antagonist, 8-cyclopentyltheophylline. In addition, hydroxylamine reversed adenosine A1 receptor-mediated inhibition of the evoked population spike, the fEPSP and the intracellularly recorded EPSP. The inhibitory modulation of adenosine A1 receptor activation by hydroxylamine suggests the presence of a potent endogenous regulatory site.
一氧化氮供体羟胺（NH2OH）可引起大鼠海马CA1区记录到的诱发突触电位出现短暂抑制。腺苷A1拮抗剂8-环戊基茶碱可消除这种抑制。此外，羟胺可逆转腺苷A1受体介导的对诱发群体峰电位、场兴奋性突触后电位（fEPSP）和细胞内记录的兴奋性突触后电位（EPSP）的抑制作用。羟胺对腺苷A1受体激活的抑制性调节提示存在一个有效的内源性调节位点。
