Sustained outward rectification of oxytocinergic neurones in the rat supraoptic nucleus: ionic dependence and pharmacology.
Sustained outward rectification of oxytocinergic neurones in the rat supraoptic nucleus: ionic dependence and pharmacology.
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大鼠视上核催产素能神经元的持续向外整流:离子依赖性和药理学。
DOI:
10.1113/jphysiol.1997.sp022036
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发表时间:
1997
期刊:
影响因子:
--
通讯作者:
Armstrong,WE
中科院分区:
文献类型:
--
作者:
Stern,JE;Armstrong,WE
1. Intracellular recordings were obtained in vitro from oxytocin and vasopressin neurones from dioestrous and lactating female rats. Oxytocin neurones were characterized under current clamp by the expression of a depolarization‐activated, sustained outward rectification (SOR) and a rebound depolarization (RD). 2. An increment in extracellular K+ shifted the expression of the SOR and RD towards a more depolarized membrane potential, indicating that the mechanisms underlying these events are dependent on extracellular potassium. 3. The SOR and RD were blocked by external tetraethylammonium (10 mM) and Ba2+ (0.1‐0.5 mM). Cs+ (2 mM) blocked the hyperpolarization‐activated inward rectification without affecting the expression of the SOR and RD. 4. The SOR was not affected by 4‐aminopyridine (6 mM). However, the rebound amplitude was significantly enhanced, indicating that the activation of a transient outward current interacts with the expression of the rebound. 5. Iberiotoxin (100 nM) and apamin (50 nM), toxins known to block some calcium‐dependent potassium conductances, did not affect the expression of the SOR and RD. 6. The SOR and RD were significantly reduced by Cd2+ (0.5 mM) but not by Ni2+ (0.25 mM). 7. Muscarine (10 microM) did not affect the SOR or the RD. 8. These results indicate that the SOR and RD depend upon a depolarization‐activated, sustained outward potassium current, which might be calcium dependent. A current with these characteristics has never been described before in the magnocellular system. Voltage‐clamp experiments are needed to completely characterize this potassium conductance selectively expressed by oxytocin neurones.
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DOI:
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发表时间:
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期刊:
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影响因子:
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作者:
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期刊:
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影响因子:
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通讯作者:
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影响因子:
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发表时间:
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期刊:
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