GABAergic synaptic transmission in projections from the basal forebrain and hippocampal formation to the amygdala: an in vivo iontophoretic study.
GABAergic synaptic transmission in projections from the basal forebrain and hippocampal formation to the amygdala: an in vivo iontophoretic study.
复制标题
从基底前脑和海马结构到杏仁核的投射中的 GABA 能突触传递：一项体内离子电渗研究。
DOI：
10.1016/0006-8993(92)91426-f
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发表时间：
1992
期刊：
影响因子：
2.9
通讯作者：
Finch,DM
中科院分区：
文献类型：
--
作者：
Mello,LE;Tan,AM;Finch,DM
我们记录了电刺激基底前脑和海马结构后大鼠杏仁核神经元的细胞外反应。离子电渗应用GABA A受体拮抗剂荷包牡丹碱，导致出现短潜伏期诱发的爆发后，刺激任何地区。无论基线反应是抑制性还是兴奋性，都会发生这种情况。荷包牡丹碱只影响抑制的早期阶段，留下更长的潜伏期，更长的持续时间相不变，甚至增加。相比之下，GABA受体拮抗剂法氯芬从未产生过如此短的潜伏期诱发爆发。荷包牡丹碱和法克氯芬都能增加杏仁核神经元的自发放电率。CNQX（AMPA亚型谷氨酸受体拮抗剂）可阻断杏仁核候选抑制神经元对海马结构刺激的兴奋性爆发反应。基于这些和先前的研究，海马结构刺激的作用似乎是由前馈抑制介导的，其中GABA能杏仁抑制性神经元被海马结构的突触能投射所兴奋。基底前脑刺激的作用可能由前馈抑制和直接GABA能抑制介导。
We recorded extracellular responses from rat amygdaloid neurons in vivo after electrical stimulation of the basal forebrain and hippocampal formation. Iontophoretic application of the GABAAreceptor antagonist, bicuculline, lead to the appearance of short latency evoked bursts after stimulation of either region. This occurred whether the baseline response was inhibitory or excitatory. Bicuculline only affected an early phase of inhibition, leaving a longer latency, longer duration phase unchanged or even increased. By contrast, the GABABreceptor antagonist, phaclofen, never produced such short latency evoked bursts. Both bicuculline and phaclofen increased the spontaneous rate of firing of amygdaloid neurons. The excitatory burst response to hippocampal formation stimulation of an amygdaloid candidate inhibitory neuron was blocked by CNQX (an antagonist of the AMPA subtype of glutamate receptor). Based on these and prior studies, it seems likely that the effects of hippocampal formation stimulation are mediated by feed-forward inhibition, in which GABAergic amygdaloid inhibitory neurons are excited by glutamatergic projections from the hippocampal formation. The effects of basal forebrain stimulation may be mediated by both feed-forward inhibition and direct, GABAergic inhibition.