Potapov A A
Neirofiziologiia. 1987;19(1):12-20.
The effects of 4-aminopyridine (10(-2) mol/l), aminooxyacetic acid (AOAA, 10(-4)-10(-3) mol/l), beta-alanine (10(-3)-10(-2) mol/l) and bicuculline (10(-5), 10(-4) mol/l) applications on the frog olfactory bulb (OB) were studied in vivo. The suppression of the orthodromic potential postsynaptic components evoked by a puff on the olfactory mucosa (OB input inhibition), or by single electrostimulation of the olfactory nerve (postsynaptic inhibition) was evaluated. 4-aminopyridine greatly reduced the OB input inhibition and strongly increased the postsynaptic inhibition. AOAA and bicuculline increased and beta-alanine slightly reduced the OB input inhibition. Clear-cut, simple alterations of the postsynaptic inhibition under the influence of the same drugs were not observed. The results confirm the hypothesis, that the OB input inhibition evoked by a puff on the olfactory mucosa may appear due to the release of GABA from glial cells and its binding with presynaptic GABAB-receptors in glomeruli.
在活体状态下研究了4-氨基吡啶（10⁻²mol/L）、氨氧基乙酸（AOAA，10⁻⁴ - 10⁻³mol/L）、β-丙氨酸（10⁻³ - 10⁻²mol/L）和荷包牡丹碱（10⁻⁵、10⁻⁴mol/L）作用于青蛙嗅球（OB）的效果。评估了由嗅黏膜上的一次吹气（OB输入抑制）或嗅神经的单次电刺激（突触后抑制）所诱发的顺行性电位突触后成分的抑制情况。4-氨基吡啶极大地降低了OB输入抑制，并强烈增强了突触后抑制。AOAA和荷包牡丹碱增加了OB输入抑制，而β-丙氨酸则略微降低了OB输入抑制。在相同药物影响下，未观察到突触后抑制有明显、简单的改变。这些结果证实了如下假说，即由嗅黏膜上的一次吹气所诱发的OB输入抑制可能是由于胶质细胞释放γ-氨基丁酸（GABA）并使其与肾小球中的突触前GABAB受体结合所致。
