Calabresi P, Ascone C M, Centonze D, Pisani A, Sancesario G, D'Angelo V, Bernardi G
Clinica Neurologica, Dip. Sanitá, Universitá di Roma Tor Vergata, 00173 Rome, Italy.
J Neurosci. 1997 Mar 15;17(6):1940-9. doi: 10.1523/JNEUROSCI.17-06-01940.1997.
We have studied the electrophysiological effects of glucose deprivation on morphologically identified striatal neurons recorded from a corticostriatal slice preparation. The large majority of the recorded cells were spiny neurons and responded to aglycemia with a slow membrane depolarization coupled with a reduction of the input resistance. In voltage-clamp experiments aglycemia caused an inward current. This current was associated with a conductance increase and reversed at -40 mV. The aglycemia-induced membrane depolarization was not affected by tetrodotoxin (TTX) or 6-cyano-7-nitroquinoxaline-2,3-dione plus aminophosphonovalerate, antagonists acting respectively on AMPA and NMDA glutamate receptors. Also, the intracellular injection of bis(2-aminophenoxy)ethane-N,N, N',N'-tetra-acetic acid, a calcium (Ca2+) chelator, and low Ca2+/high Mg2+-containing solutions failed to reduce this phenomenon. Conversely, it was reduced by lowering external sodium (Na+) concentration. A minority of the recorded cells had the morphological characteristics of large aspiny interneurons and the electrophysiological properties of "long-lasting afterhyperpolarization (LA) cells." These cells responded to aglycemia with a membrane hyperpolarization/outward current that was coupled with an increased conductance. This current was not altered by TTX, blockers of ATP-dependent potassium (K+) channels, and adenosine A1 receptor antagonists, whereas it was reduced by solutions containing low Ca2+/high Mg2+. This current reversed at -105 mV and was blocked by barium, suggesting the involvement of a K+ conductance. We suggest that the opposite membrane responses of striatal neuronal subtypes to glucose deprivation might account for their differential neuronal vulnerability to aglycemia and ischemia.
我们研究了葡萄糖剥夺对从皮质纹状体脑片制备中记录的形态学鉴定的纹状体神经元的电生理效应。记录的细胞绝大多数是棘状神经元，对无糖血症的反应是缓慢的膜去极化，同时输入电阻降低。在电压钳实验中，无糖血症引起内向电流。该电流与电导增加相关，并在 -40 mV 时反转。无糖血症诱导的膜去极化不受河豚毒素（TTX）或 6-氰基-7-硝基喹喔啉-2,3-二酮加氨基膦酸戊酯的影响，这两种拮抗剂分别作用于 AMPA 和 NMDA 谷氨酸受体。此外，细胞内注射双（2-氨基苯氧基）乙烷-N,N,N',N'-四乙酸（一种钙螯合剂）以及含低钙/高镁的溶液未能减少这种现象。相反，通过降低细胞外钠（Na+）浓度可使其减少。少数记录的细胞具有大的无棘中间神经元的形态特征和“持久超极化后电位（LA）细胞”的电生理特性。这些细胞对无糖血症的反应是膜超极化/外向电流，同时电导增加。该电流不受 TTX、ATP 依赖性钾（K+）通道阻滞剂和腺苷 A1 受体拮抗剂的影响，而含低钙/高镁的溶液可使其减少。该电流在 -105 mV 时反转，并被钡阻断，提示涉及一种 K+ 电导。我们认为纹状体神经元亚型对葡萄糖剥夺的相反膜反应可能解释了它们对无糖血症和缺血的不同神经元易损性。
