Nakahiro M, Saito K, Yamada I, Yoshida H
Neurosci Lett. 1985 Jun 24;57(3):263-6. doi: 10.1016/0304-3940(85)90502-6.
The effect of delta-aminovaleric acid (delta-AV) on bicuculline-insensitive gamma-aminobutyric acid B (GABA B) sites in the central nervous system (CNS) was investigated by binding studies and experiments on slices in vitro. delta-AV inhibited [3H]GABA (10 nM) binding to GABA B sites in a rat brain membrane preparation with an IC50 value of 10(-4) M. It also inhibited [3H]baclofen (20 nM) binding with an IC50 value of 10(-4) M. In preparations of hippocampal slices, (-)-baclofen (5 microM) reduced the population spikes evoked by stimulating the Schaffer collaterals in CA1 pyramidal cells in the presence of 100 microM bicuculline. delta-AV (1 mM) antagonized this inhibitory action of baclofen. Since baclofen is an agonist of GABAB sites, our results indicate that delta-AV has an antagonistic effect on GABAB sites in the CNS.
通过结合研究和体外脑片实验，研究了δ-氨基戊酸（δ-AV）对中枢神经系统（CNS）中对荷包牡丹碱不敏感的γ-氨基丁酸B（GABAB）位点的影响。δ-AV抑制大鼠脑膜制剂中[3H]GABA（10 nM）与GABAB位点的结合，IC50值为10(-4) M。它还抑制[3H]巴氯芬（20 nM）的结合，IC50值为10(-4) M。在海马脑片制剂中，（-）-巴氯芬（5 microM）在存在100 microM荷包牡丹碱的情况下，减少了刺激CA1锥体细胞中Schaffer侧支所诱发的群体峰电位。δ-AV（1 mM）拮抗了巴氯芬的这种抑制作用。由于巴氯芬是GABAB位点的激动剂，我们的结果表明δ-AV对中枢神经系统中的GABAB位点具有拮抗作用。
