Tuff L P, Racine R J, Adamec R
Brain Res. 1983 Oct 24;277(1):79-90. doi: 10.1016/0006-8993(83)90909-5.
Double-pulse stimulation of the perforant path input to the dentate gyrus was used in the following experiments to produce paired pulse depression in that site. This effect provided an estimate of GABA-mediated recurrent inhibition. The depression was enhanced by drugs that facilitate or mimic GABA action and attenuated by drugs which block GABA transmission. Paired-pulse depression was significantly increased following amygdala kindling and was further enhanced to near maximal levels by subsequent kindling in the dentate. In addition, kindling did not increase the rate at which inhibition failed under conditions of excessive activation. Trains of 5 Hz stimulation, applied to the perforant path, caused paired-pulse depression to disappear and elicited a brief AD. Following kindling, the latency to AD onset tended to be increased rather than shortened, suggesting an enhanced resistance to inhibitory failure. These results indicated that kindling increased, rather than reduced, inhibition in the dentate gyrus.
在以下实验中，使用对齿状回的穿通通路输入进行双脉冲刺激，以在该部位产生双脉冲抑制。这种效应提供了GABA介导的反馈抑制的估计。促进或模拟GABA作用的药物会增强这种抑制，而阻断GABA传递的药物会减弱这种抑制。杏仁核点燃后，双脉冲抑制显著增加，随后齿状回点燃会进一步增强至接近最大水平。此外，在过度激活的条件下，点燃并没有增加抑制失败的速率。施加于穿通通路的5Hz刺激串导致双脉冲抑制消失并引发短暂的强直性放电。点燃后，强直性放电开始的潜伏期往往增加而不是缩短，表明对抑制失败的抵抗力增强。这些结果表明，点燃增加而非减少了齿状回中的抑制作用。
