Solís J M, Nicoll R A
Department of Pharmacology, University of Califoria, San Francisco 91413-0450.
Neurosci Lett. 1992 Nov 23;147(1):16-20. doi: 10.1016/0304-3940(92)90764-x.
Intracellular and whole-cell recording from CA1 pyramidal cells and dentate granule cells was used to study the release of endogenous GABA by nipecotic acid. Local application of nipecotic acid produced responses that could be entirely blocked by a combination of the GABAA receptor antagonist picrotoxin and the GABAB receptor antagonist CGP 35348. These responses were due to the heteroexchange release of endogenous GABA because they were blocked by low Na+ which blocks the GABA transporter and by SKF 89976 which is a competitive antagonist of the GABA transporter. Local application of nipecotic acid could, depending on the location, evoke pure GABAA or pure GABAB responses supporting proposals that GABAA and GABAB receptors can be segregated at separate inhibitory synapses.
采用从CA1锥体细胞和齿状颗粒细胞进行细胞内和全细胞记录的方法,研究了尼克酸对内源性γ-氨基丁酸(GABA)释放的影响。局部应用尼克酸产生的反应可被GABAA受体拮抗剂印防己毒素和GABAB受体拮抗剂CGP 35348联合完全阻断。这些反应是由于内源性GABA的异质交换释放,因为它们被阻断GABA转运体的低钠以及GABA转运体的竞争性拮抗剂SKF 89976所阻断。根据位置不同,局部应用尼克酸可诱发纯GABAA或纯GABAB反应,这支持了GABAA和GABAB受体可在不同抑制性突触处分离的观点。