Yasuda R P, Zahniser N R, Dunwiddie T V
Neurosci Lett. 1984 Mar 23;45(2):199-204. doi: 10.1016/0304-3940(84)90099-5.
The effects of cocaine on electrophysiological activity were examined in the CA1 region of the in vitro hippocampal slice. Low concentrations of cocaine (0.25-2.5 microM) had no direct effect on evoked potentials, but potentiated responses to threshold concentrations of norepinephrine (NE; 0.5 microM); this effect was also seen with other inhibitors of catecholamine uptake such as desipramine. The ability of low doses of cocaine to augment the changes in population spike amplitude elicited by NE appeared to be related to the ability of cocaine to block the uptake of NE into the noradrenergic nerve terminals in the rat hippocampus. Higher concentrations of cocaine (5-200 microM) elicited responses consistent with local anesthetic actions on neuronal membranes.
在体外海马切片的CA1区检测了可卡因对电生理活动的影响。低浓度可卡因（0.25 - 2.5微摩尔）对诱发电位无直接作用，但增强了对阈浓度去甲肾上腺素（NE；0.5微摩尔）的反应；其他儿茶酚胺摄取抑制剂如地昔帕明也有此作用。低剂量可卡因增强NE引起的群体峰电位幅度变化的能力，似乎与可卡因阻断NE摄取到大鼠海马去甲肾上腺素能神经末梢的能力有关。较高浓度的可卡因（5 - 200微摩尔）引起的反应与局部麻醉药对神经元膜的作用一致。
