Co-release of noradrenaline and dopamine in the prefrontal cortex after acute morphine and during morphine withdrawal
Co-release of noradrenaline and dopamine in the prefrontal cortex after acute morphine and during morphine withdrawal
复制标题
DOI：
10.1007/s00213-001-0985-y
复制
发表时间：
2002-03-01
影响因子：
3.4
通讯作者：
Gessa, GL
中科院分区：
文献类型：
--
作者：
Devoto, P;Flore, G;Gessa, GL
基本原理：急性吗啡和慢性吗啡戒断已被证明增加和减少细胞外多巴胺（DA）在延髓核，分别。与此相反，细胞外DA在前额叶皮层（PFC）是不修改的急性吗啡，并显着增加戒断综合征。目的：我们调查是否PFC DA的特殊行为可能取决于这样一个事实，即细胞外DA不仅来自DA，但主要是去甲肾上腺素（NA）终端。因此，我们研究了急性吗啡和吗啡戒断的效果是否通过抑制DA或NA神经元来改变。研究方法：细胞外DA和去甲肾上腺素（NA）的浓度测定微透析PFC（密集神经支配的DA）和顶叶皮质（缺乏DA传入）后，急性吗啡和吗啡依赖大鼠在纳洛酮沉淀戒断综合征。通过高效液相色谱法（HPLC）和电化学检测评价透析液中的儿茶酚胺水平。结果如下：急性吗啡（5毫克/公斤IP）减少细胞外NA（30%），并未能修改细胞外DA水平的PFC，但减少了40%的两种胺在顶叶皮层。吗啡和D1激动剂喹吡罗的联合给药腹腔注射纳洛酮（0.5mg/kg）可使PFC细胞外DA和NA降低40%。（1.0 mg/kg，SC）引起典型的戒断综合征，伴随细胞外DA和NA分别显著增加约200和100%，α 2肾上腺素受体激动剂可乐定（0.15 mg/kg IP）抑制纳洛酮诱发的戒断症状，并使PFC中的NA和DA输出增加，
Rationale: Acute morphine and abstinence from chronic morphine have been shown to increase and to decrease extracellular dopamine (DA) in the nucleus accumbens, respectively. In contrast, extracellular DA in the prefrontal cortex (PFC) is not modified by acute morphine and is markedly increased during abstinence syndrome. Objectives: We investigated whether the peculiar behaviour of PFC DA might depend on the fact that extracellular DA originates not only from DA but, mainly, noradrenaline (NA) terminals. Accordingly, we studied if the effect of acute morphine and morphine-abstinence was modified by the inhibition of DA or NA neurons. Methods: Extracellular DA and noradrenaline (NA) concentrations were determined by microdialysis in the PFC (densely innervated by DA) and in the parietal cortex (lacking DA afferents) both after acute morphine and in morphine-dependent rats during naloxone-precipitated abstinence syndrome. Dialysate catecholamine levels were evaluated by high performance liquid chromatography (HPLC) with electrochemical detection. Results: Acute morphine (5 mg/kg IP) reduced extracellular NA (by 30%) and failed to modify extracellular DA level in the PFC, but reduced both amines by 40% in the parietal cortex. The co-administration of morphine and the D, agonist quinpirole (0.5 mg/kg IP) decreased both extracellular DA and NA by 40% in the PFC. In morphine dependent rats the administration of naloxone (1.0 mg/kg, SC) precipitated a typical abstinence syndrome associated with a concomitant dramatic increase in extracellular DA and NA by about 200 and 100%, respectively, in the PFC. The alpha(2)-adrenoceptor agonist clonidine (0.15 mg/kg IP) suppressed naloxone precipitated abstinence symptoms and brought both NA and DA output in the PFC to