Role of large conductance calcium-activated potassium channels in neuronal Ca2+ overload following traumatic brain injury
10.3760/cma.j.issn.1001-8050.2010.12.026
- VernacularTitle:创伤性脑损伤神经细胞钙超载机制中大电导钙激活钾通道的作用
- Author:
Hong ZHAO
;
Wenhua YANG
;
Xiangjun BAI
- Publication Type:Journal Article
- Keywords:
Brain injuries;
Neuron;
Calcium;
Large conductance calcium-activated potassium channel
- From:
Chinese Journal of Trauma
2010;26(12):1140-1143
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the role of large conductance calcium-activated potassium channels (BK) in neuronal Ca2+ overload following traumatic brain injury (TBI). Methods Neuronal cells of C57BL/6 mouse cortex were collected and cultured. Patch-clamp technique was applied to investigate the changes of intracellular free calcium [Ca2+] i and firing frequency of neuronal action potentials in rest condition or evoked by 100 pA electric current lasting 500 ms after perfusion of Iberiotoxin ( 100 nmmol/L), a BK specific blocker. The cells were divided randomly into experimental group ( plus Iberiotoxin) and control group. Extracellular solution of cultured neurons was further perfused with KCl (20 mmol/L) to induce elevation of [Ca2 +]i and influence of Iberiotoxin ( 100 nmol/L) on amplitude of [Ca2 +] i elevation was determined. Results No significant changes of neuronal spontaneous action potential frequency and [Ca2 +]i were observed in rest condition after perfusion of Iberiotoxin (P＞0.05).However, when evoked by electric current, the frequency of action potential was (10.4 ± 3.0) Hz,which was increased to ( 13.8 ± 3.7 ) Hz after perfusion of Iberiotoxin, with statistical difference (P＜0.05 ). The [Ca2 +] i level was ( 14.21 ± 16.98 ) nmol/Lbefore perfusion with Iberiotoxin but was increased to (44.07 ± 34. 4) nmol/L after perfusion of Iberiotoxin (P ＜ 0.05 ). Extracellular high concentration of KCl increased [Ca2 +] i of neurons, while perfudion of Iberiotoxin further elevated [Ca2 +]i (P ＜ 0.05).Conclusion BK may play an important role in the regulation of neuronal [Ca2+] i and in neuronal Ca2+overload following TBI.
