Chang A Y, Kuo T B, Tsai T H, Chen C F, Chan S H
Center for Neuroscience, National Yang-Ming University, Taipei, Taiwan, Republic of China.
Synapse. 1995 Oct;21(2):149-57. doi: 10.1002/syn.890210208.
We applied continuous, on-line and real-time spectral analysis of electroencephalographic (EEG) signals and microdialysis to evaluate the possible participation of noradrenergic neurotransmission at the medial prefrontal cortex (mPFC) in EEG desynchronization induced by cocaine. Male Sprague-Dawley rats that were under chloral hydrate anesthesia were used. Intravenous administration of cocaine (1.5 or 3.0 mg/kg) dose-dependently induced EEG desynchronization, as represented by a decrease in root mean square (RMS) and an increase in mean power frequency (MPF) value of the EEG signals. Power spectral analysis further revealed that whereas both doses of cocaine promoted a reduction in the alpha (8-13 Hz), theta (4-8 Hz), and delta (1-4 Hz) components, the lower dose of cocaine decreased, and the higher dose increased the beta band (13-32 Hz). Microdialysis data indicated an elevation in extracellular concentration of norepinephrine at the mPFC that paralleled temporally and correlated positively with the maximal effect of cocaine on EEG activity. Bilateral microinjection of the selective noradrenergic neurotoxin, DSP4 (50 micrograms), or equimolar concentration (500 pmol) of the alpha 1-adrenoceptor antagonist, prazosin, or alpha 2-adrenoceptor antagonist, yohimbine, into the mPFC significantly blunted the decrease in delta component (prazosin) or both delta and theta components (DSP4 or yohimbine) of EEG activity by the lower dose of cocaine. On the other hand, the same pretreatments appreciably antagonized the increase in beta band by cocaine at 3.0 mg/kg. The potency of the antagonism by yohimbine, however, was higher than prazosin. These results suggest that cocaine may elicit EEG desynchronization via noradrenergic neurotransmission, and that alpha 2-adrenoceptors, and to a lesser extent, alpha 1-adrenoceptors, at the mPFC may be involved in the subtle dose-dependent changes in individual EEG spectral components.
我们应用脑电图（EEG）信号的连续、在线和实时频谱分析以及微透析技术，来评估去甲肾上腺素能神经传递在中前额叶皮质（mPFC）对可卡因诱导的EEG去同步化过程中可能发挥的作用。实验使用了水合氯醛麻醉下的雄性Sprague-Dawley大鼠。静脉注射可卡因（1.5或3.0毫克/千克）剂量依赖性地诱导EEG去同步化，表现为EEG信号的均方根（RMS）降低和平均功率频率（MPF）值增加。功率谱分析进一步显示，两种剂量的可卡因均促使α（8 - 13赫兹）、θ（4 - 8赫兹）和δ（1 - 4赫兹）成分减少，而较低剂量的可卡因使β波段（13 - 32赫兹）减少，较高剂量则使其增加。微透析数据表明，mPFC处去甲肾上腺素的细胞外浓度升高，其在时间上与可卡因对EEG活动的最大效应平行且呈正相关。向mPFC双侧微量注射选择性去甲肾上腺素能神经毒素DSP4（50微克），或等摩尔浓度（500皮摩尔）的α1 - 肾上腺素能受体拮抗剂哌唑嗪，或α2 - 肾上腺素能受体拮抗剂育亨宾，可显著减弱较低剂量可卡因引起的EEG活动δ成分（哌唑嗪）或δ和θ成分（DSP4或育亨宾）的减少。另一方面，相同的预处理明显拮抗了3.0毫克/千克可卡因引起的β波段增加。然而，育亨宾的拮抗效力高于哌唑嗪。这些结果表明，可卡因可能通过去甲肾上腺素能神经传递引发EEG去同步化，并且mPFC处的α2 - 肾上腺素能受体以及程度较轻的α1 - 肾上腺素能受体可能参与了个体EEG频谱成分中细微的剂量依赖性变化。
