REGULATION OF DOPAMINE RELEASE BY IMPULSE FLOW AND BY AUTORECEPTORS AS STUDIED BY INVIVO VOLTAMMETRY IN THE RAT STRIATUM
REGULATION OF DOPAMINE RELEASE BY IMPULSE FLOW AND BY AUTORECEPTORS AS STUDIED BY INVIVO VOLTAMMETRY IN THE RAT STRIATUM
复制标题
DOI：
10.1016/0306-4522(85)90141-1
复制
发表时间：
1985-01-01
期刊：
影响因子：
3.3
通讯作者：
BUDA, MJ
中科院分区：
文献类型：
--
作者：
GONON, FG;BUDA, MJ
用差示正常脉冲伏安法监测帕格林处理的麻醉大鼠脑组织细胞外多巴胺[DA]浓度。当6-羟基多巴胺选择性破坏多巴胺能终末时，经电化学处理的碳纤维电极记录的儿茶酚氧化电流消失。基础氧化电流的校正表明，细胞外DA浓度为26 nM。在前脑内侧束水平对黑质纹状体通路进行短暂和适度的电刺激，可引起DA电流的显著增加。观察到的DA信号升高的持续时间与刺激的时间一样长。它随脉冲频率(0-25赫兹)呈指数变化。以突发模式分布的刺激脉冲的效力是相同数量规则间隔的脉冲的两倍。用未经处理的碳纤维电极对麻醉大鼠(不含帕吉林)也进行了高频刺激(50赫兹)；它们引起非常大的细胞外Da浓度的增加(高达8-15微米)。用电解性损毁或小剂量阿朴吗啡(0.05 mg kg)阻断多巴胺能冲动流可立即引起DA电流的降低。这些效应的时间进程和幅度(-70%)是相同的。随后注射氟哌啶醇(0.5 mg kg)可逆转阿朴吗啡效应，最高可达对照基础值的+360%。多巴胺能拮抗剂氟哌啶醇(0.05和0.5 mg kg)或甲氧氯普胺(2 Mg Kg)显著增加DA电流，分别为对照组的317、340和215%。诺米芬新(4 mg·kg-1)使细胞外多巴胺水平显著升高(+417%)。电刺激多巴胺能通路的效应可被苯丙胺(2 Mg Kg)、诺米芬新(4 Mg Kg)或氟哌啶醇(0.05和0.5 mg kg)等药物增强，但不被阿朴吗啡(0.05 mg kg)所改变。DA的释放既受脉冲频率的影响，也受纹状体多巴胺能自身受体频率的影响。
Extracellular dopamine [DA] concentration was monitored in the stratum of parglyline-treated, anesthetized rats using differential normal pulse voltammetry. The catechol oxidation current recorded with electrochemically treated carbon fiber electrodes disappeared when the dopaminergic terminals were selectively destroyed by 6-hydroxydopamine. Calibration of the basal oxidation current revealed that the extracellular DA concentration was 26 nM. Brief and moderate electrical stimulation of the nigrostriatal pathway at the level of the medial forebrain bundle induced a large increase in the DA current. The observed elevation in the DA signal lasted as long as the stimulation. It varied with the frequency (0-25 Hz) of the pulses in an exponential manner. Stimulation pulses distributed in a bursted pattern were twice as potent as an equivalent number of pulses regularly spaced. High frequency stimulations (50 Hz) were also investigated in anesthetized rats (without pargyline) with untreated carbon fiber electrodes; they induced a very large increase in the Da extracellular concentration (up to 8-15 .mu.M). Interruption of the dopaminergic impulse flow either by an electrolytic lesion or by a low dose of apomorphine (0.05 mg kg) caused an immediate decrease of the DA current. The time courses and amplitudes (-70%) of these effects were identical. Subsequent injection of haloperidol (0.5 mg kg) reversed the apomorphine effect up to +360% of the control basal value. Administration of dopaminergic antagonists such as haloperidol (0.05 and 0.5 mg kg) or metoclopramide (2 mg kg) significantly increased the DA current up to 317, 340 and 215% of the respective control values. Nomifensine (4 mg kg) produced a big increase (+417%) of the extracellular DA levels. The effect of electrical stimulation of the dopaminergic pathway was potentiated by drugs such as amphetamine (2 mg kg), nomifensine (4 mg kg) or haloperidol (0.05 and 0.5 mg kg) but was not altered by apomorphine (0.05 mg kg). The release of DA is under the influence of both the frequency of impulse flow and of dopaminergic striatal autoreceptors.