Carta Mario, Olivera Dorian S, Dettmer Todd S, Valenzuela C Fernando
Department of Neurosciences, University of New Mexico Health Sciences Center, Albuquerque, NM 87131-5223, USA.
Neurosci Lett. 2002 Jul 19;327(2):128-32. doi: 10.1016/s0304-3940(02)00399-3.
We have previously demonstrated that kainate receptors (KA-Rs) are acutely inhibited by ethanol (EtOH). Here we show that KA-Rs are also affected by long-term EtOH exposure. Whole-cell recordings of pharmacologically isolated KA-R-mediated currents in cultured hippocampal neurons revealed that exposure to 80 mM EtOH for 3 days followed by a 24 h withdrawal period increased KA-R current densities. Quantitative confocal microscopy showed that expression of GluR6/7 subunits increases after ethanol withdrawal in these neurons. Since KA-Rs control hippocampal excitability and seizure generation, we postulate that upregulation of these receptors may have a role in the pathophysiology of alcohol withdrawal syndrome.
我们之前已经证明，海藻酸受体（KA-Rs）会被乙醇（EtOH）急性抑制。在此我们表明，KA-Rs也会受到长期EtOH暴露的影响。对培养的海马神经元中经药理学分离的KA-R介导电流进行的全细胞记录显示，暴露于80 mM EtOH 3天，随后经过24小时戒断期，KA-R电流密度增加。定量共聚焦显微镜检查表明，在这些神经元中，乙醇戒断后GluR6/7亚基的表达增加。由于KA-Rs控制海马的兴奋性和癫痫发作的产生，我们推测这些受体的上调可能在酒精戒断综合征的病理生理学中起作用。
