Hypocretin/orexin depolarizes and decreases potassium conductance in locus coeruleus neurons
Hypocretin/orexin depolarizes and decreases potassium conductance in locus coeruleus neurons
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DOI：
10.1097/00001756-200006050-00031
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发表时间：
2000-06-05
期刊：
影响因子：
1.7
通讯作者：
Aston-Jones, G
中科院分区：
文献类型：
--
作者：
Ivanov, A;Aston-Jones, G
最近的研究表明，去甲肾上腺素能蓝斑（LC）神经元是一个特别强的新的神经肽，下丘脑泌素（食欲素）的目标。本研究旨在阐明的行动，hypocretin-B（HCRT）对LC神经元的细胞内记录在大鼠脑片。在大鼠脑切片中，HCRT的浴（1.0 μ M）或局部抽吸应用（50-100 μ M，在移液管中）使LC神经元去极化，并增加其自发放电率。HCRT诱发的去极化是持久的河豚毒素（TTX，1 μ M）和钴+（1 mM）的存在下，表明HCRT直接激活LC神经元，其对突触后细胞的影响是不是由于TTX敏感的钠通道或钴+敏感的钙通道的激活。在HCRT诱发的去极化过程中，大多数LC神经元的表观输入电阻显著增加。HCRT诱发的去极化幅度随膜超极化而降低。本研究结果表明，降低钾电导参与HCRT对LC神经元的影响。NeuroReport 11：1755-1758（C）2000 Lippincott威廉姆斯和威尔金斯。
Recent studies demonstrated that noradrenergic locus coeruleus (LC) neurons are a particularly strong target of the novel neuropeptide, hypocretin (orexin). The present study sought to elucidate the action of hypocretin-B (HCRT) on LC neurons recorded intracellularly in rat brain slices. Bath (1.0 mu M) or local puff application (50-100 mu M in pipette) of HCRT depolarized LC neurons in rat brain slices and increased their spontaneous discharge rate. Depolarization evoked by HCRT was persistent in the presence of tetrodotoxin (TTX, 1 mu M) and Co2+ (1 mM), indicating that HCRT directly activated LC neurons, and that its effect on the postsynaptic cell was not due to activation of TTX-sensitive sodium channels or Co2+-sensitive calcium channels. The apparent input resistance was significantly increased in the majority of LC neurons during the HCRT-evoked depolarization. Moreover, the HCRT-evoked depolarization was decreased in amplitude with hyperpolarization of membrane. The present results indicate that decreased potassium conductance is involved in the effect of HCRT on LC neurons. NeuroReport 11:1755-1758 (C) 2000 Lippincott Williams & Wilkins.