Zhang Chun-xiao, Zhang Wen-jie, Liu Yong-feng, Wang Shao
Department of Physiology, School of Basic Medical Sciences, Jilin University, Changchun 13021, China.
Zhongguo Ying Yong Sheng Li Xue Za Zhi. 2007 Nov;23(4):442-5.
To investigate the effects and the possible mechanism of cocaine on the neurons of lateral habenular nucleus (LHb).
We observed the effects on c-Fos protein expression in lateral habenular nucleus and medial habenular nucleus after injecting cocaine into a belly cavity and spontaneous and evoked discharge of pain-correlative unit through iontophoresis of cocaine into LHb. The delayed rectifier K+ current was recorded in the acute isolated LHb neuron in whole-cell mode.
(1) The c-Fos protein expression was increased by cocaine treatment in LHb, but little effect in MHb. (2) Iontophoresis of cocaine into LHb increased the discharges of pain excitation unit and enhanced excitation response to noxious stimulation, but it decreased the discharges of pain inhibition unit and its responses to noxious stimulation in LHb. Cocaine inhibited the delayed rectifier K+ current.
Cocaine can excite the LHb and increase its sensitivity. The probable mechanism is that cocaine inhibits the delayed rectifier K+ channels.
研究可卡因对外侧缰核（LHb）神经元的作用及其可能机制。
通过腹腔注射可卡因观察其对外侧缰核和内侧缰核中c-Fos蛋白表达的影响，并通过向LHb离子导入可卡因观察疼痛相关单位的自发放电和诱发放电。采用全细胞模式记录急性分离的LHb神经元的延迟整流钾电流。
（1）可卡因处理可使LHb中c-Fos蛋白表达增加，而对内侧缰核（MHb）影响较小。（2）向LHb离子导入可卡因可增加疼痛兴奋单位的放电，并增强对有害刺激的兴奋反应，但可减少LHb中疼痛抑制单位的放电及其对有害刺激的反应。可卡因抑制延迟整流钾电流。
可卡因可兴奋LHb并增加其敏感性。可能机制是可卡因抑制延迟整流钾通道。
