POTASSIUM-DEPENDENT CALCIUM INFLUX IN ACUTELY ISOLATED HIPPOCAMPAL ASTROCYTES
POTASSIUM-DEPENDENT CALCIUM INFLUX IN ACUTELY ISOLATED HIPPOCAMPAL ASTROCYTES
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DOI：
10.1016/0306-4522(94)90059-0
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发表时间：
1994-07-01
期刊：
影响因子：
3.3
通讯作者：
MACVICAR, BA
中科院分区：
文献类型：
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作者：
DUFFY, S;MACVICAR, BA
钾去极化可以增加培养的星形胶质细胞内钙离子浓度([Ca~(2+)](I))，但在完整的中枢神经系统中成熟的星形胶质细胞是否也表现出电压依赖性的[Ca~(2+)](I)信号尚不清楚。为了解决这一问题，从幼年大鼠海马区急性分离的星形胶质细胞中进行了[Ca~(2+)](I)的荧光测量。对照组含5 mM[K+](0)的人工脑脊液，静息[Ca~(2+)](I)平均为195 nM。[K+](0)升高至50 mm时，[Ca~(2+)](I)较静息水平升高150 NM至1微米。引起[Ca~(2+)](I)升高所需的[K~+](0)阈值为20-25 mm，[Ca~(2+)](I)信号的大小随着[K~+](0)的增加而逐渐增大(直到50 mm)。这些[Ca~(2+)](I)升高可被外源性Ca~(2+)完全阻断，并被钙通道阻滞剂维拉帕米(30 mM及以上)和CO~(2+)(1 MM)显著抑制。Na~+-Ca~(2+)交换的逆转，或Ca~(2+)激活的Ca~(2+)释放，或通过牵张激活通道的Ca~(2+)内流，均未引起[Ca~(2+)](I)的升高。这些结果表明，[K+](0)诱发的[Ca~(2+)](I)信号是通过电压门控钙通道内流介导的。与培养的星形胶质细胞和急性分离的神经元相比，这些[Ca~(2+)](I)的增加对二氢吡啶化合物不敏感。我们认为，在几种病理条件下原位观察到的间质[K+]的增加，触发了星形胶质细胞的电压依赖性[Ca~(2+)](I)信号。这可能构成了神经元-神经胶质通讯的一种重要形式。
Potassium depolarization can increase the intracellular ionized calcium concentration ([Ca2+](i)) of cultured astrocytes, but it is not known if astrocytes that have matured in the intact CNS also exhibit voltage-dependent [Ca2+](i) signalling. To address this issue, fluorometric measurements of [Ca2+](i) were obtained from astrocytes acutely isolated from young adult rat hippocampus. In control artificial cerebrospinal fluid containing 5 mM [K+](0), average resting [Ca2+](i) was 195 nM. Elevation of [K+](0) to 50 mM caused [Ca2+](i) to increase 150 nM to 1 mu M above resting levels. The threshold [K+](0) necessary to evoke an elevation in [Ca2+](i) was 20-25 mM, and the magnitude of the [Ca2+](i) signal grew progressively with increasing [K+](0) (up to 50 mM). These [Ca2+](i) increases were blocked completely by removal of external Ca2+, and markedly suppressed by the calcium channel blockers verapamil (30 mu M and greater) and Co2+ (1 mM). Neither reversal of Na+-Ca2+ exchange, nor Ca2+-activated Ca2+ release, nor Ca2+ influx through stretch-activated channels contributed to the [Ca2+](i) increase. These results suggest that [K+](0)-evoked [Ca2+](i) signals are mediated by influx through voltage-gated calcium channels. In contrast to results from cultured astrocytes and acutely isolated neurons, these [Ca2+](i) increases were insensitive to dihydropyridine compounds.We conclude that increases in interstitial [K+], observed in situ during several pathological conditions, trigger voltage-dependent [Ca-2+](i) signals in astroglial cells. This may constitute an important form of neuron-to-glial communication.