Release of Acetylcholine and Noradrenaline from the Cholinergic and Adrenergic Afferents in Rat Hippocampal CA1, CA3 and Dentate Gyrus Regions
Release of Acetylcholine and Noradrenaline from the Cholinergic and Adrenergic Afferents in Rat Hippocampal CA1, CA3 and Dentate Gyrus Regions
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大鼠海马 CA1、CA3 和齿状回区域胆碱能和肾上腺素能传入神经释放乙酰胆碱和去甲肾上腺素
DOI：
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发表时间：
1994
影响因子：
3.4
通讯作者：
E. Vizi
中科院分区：
文献类型：
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作者：
E. Milusheva;M. Baranyi;T. Zelles;A. Mike;E. Vizi
尝试研究从海马不同亚区（CA1、CA3 和齿状回）解剖的分离切片制剂中乙酰胆碱 (ACh) 和去甲肾上腺素的释放及其突触前调节。将切片灌注并加载[3H]胆碱或[3H]去甲肾上腺素。采用放射化学方法测定响应场刺激的释放情况，并通过化学发光法或高效液相色谱法结合电化学检测法测定递质的含量。 [3H]胆碱加载 30 分钟后，[3H]ACh 含量的比活性存在明显的次区域差异。在齿状回中测得浓度最高，在 CA3 中测得浓度最低。获得的证据表明，在所有三个子区域中，胆碱能轴突末端都配备有抑制性毒蕈碱自身受体，去甲肾上腺素能末端配备有α2-自身受体，当组织暴露于选择性毒蕈碱或α2-肾上腺素受体拮抗剂时，递质释放增加表明了这一点。相反，胆碱能末端不具有α2-肾上腺素受体，去甲肾上腺素能末端不具有抑制性毒蕈碱受体。因此得出的结论是，虽然乙酰胆碱和去甲肾上腺素的释放均受负反馈调节控制，但两者之间不可能建立突触前抑制相互作用。
An attempt was made to study the release of acetylcholine (ACh) and noradrenaline and their presynaptic modulation in isolated slice preparations dissected from different subfields of the hippocampus: CA1, CA3 and the dentate gyrus. The slices were perfused and loaded with [3H]choline or with [3H]noradrenaline. The release in response to field stimulation was determined radiochemically and the content of transmitters was assayed by a chemiluminescent method or by HPLC combined with electrochemical detection. After 30 min of loading with [3H]choline there were marked subregional differences in the specific activity of [3H]ACh content. The highest concentration was measured in the dentate gyrus and the lowest in CA3. Evidence was obtained that in all three subfields the cholinergic axon terminals are equipped with inhibitory muscarinic autoreceptors and the noradrenergic terminals with α2‐autoreceptors, as indicated by an increase in transmitter release when the tissue was exposed to selective muscarinic or α2‐adrenoceptor antagonists. In contrast, the cholinergic boutons are not equipped with α2‐adrenoceptors, and noradrenergic terminals do not possess inhibitory muscarinic receptors. It is therefore concluded that while the release of both ACh and noradrenaline is controlled by negative feedback modulation, there is no possibility of establishing a presynaptic inhibitory interaction between the two.