Seutin V, Johnson S W, North R A
Vollum Institute, Oregon Health Sciences University, Portland 97201.
Neuroscience. 1994 Jan;58(1):201-6. doi: 10.1016/0306-4522(94)90167-8.
Intracellular microelectrode recordings were made from dopamine-containing neurons of the ventral tegmental area or substantia nigra zona compacta in rat brain slices in vitro. The firing pattern of the neurons was switched from a tonic, single-spike pattern to a burst firing mode by adding N-methyl-D-aspartate (20 microM) to the superfusing solution; after adding tetrodotoxin the membrane potential underwent rhythmical oscillations of 20-40 mV at 0.5-2 Hz. Baclofen (1 microM) and dopamine (30 microM) hyperpolarized the neurons; when the potential was restored to its original level, the oscillations of potential and/or burst firing were not observed, but the tonic firing pattern was restored. These effects of baclofen and dopamine were prevented by barium (1 mM), which also prevented the membrane hyperpolarization. Oscillations of membrane current of a similar frequency were observed when the somatic membrane was voltage-clamped at -60 mV; these were also blocked by barium (1 mM). It is concluded that the oscillations in membrane potential observed with N-methyl-D-aspartate are generated predominantly at a dendritic location which is not voltage-clamped with an electrode at the soma. Baclofen and dopamine inhibit the oscillations by increasing the potassium conductance and hyperpolarizing the dendrites.
在体外培养的大鼠脑片中,用细胞内微电极记录腹侧被盖区或黑质致密部含多巴胺神经元的电活动。通过向灌流液中添加N-甲基-D-天冬氨酸(20微摩尔),神经元的放电模式从紧张性单峰模式转变为爆发式放电模式;添加河豚毒素后,膜电位在0.5 - 2赫兹频率下出现20 - 40毫伏的节律性振荡。巴氯芬(1微摩尔)和多巴胺(30微摩尔)使神经元超极化;当电位恢复到原始水平时,未观察到电位振荡和/或爆发式放电,但紧张性放电模式得以恢复。钡(1毫摩尔)可阻止巴氯芬和多巴胺的这些作用,同时也能阻止膜超极化。当细胞膜在 - 60毫伏电压钳制时,观察到类似频率的膜电流振荡;这些振荡也被钡(1毫摩尔)阻断。由此得出结论,N-甲基-D-天冬氨酸诱导的膜电位振荡主要产生于树突部位,该部位未被位于胞体的电极进行电压钳制。巴氯芬和多巴胺通过增加钾电导并使树突超极化来抑制振荡。