Mana M J, Grace A A
Department of Neuroscience, University of Pittsburgh, PA 15260, USA.
Neuroscience. 1997 Dec;81(4):1055-64. doi: 10.1016/s0306-4522(97)00225-x.
In vivo extracellular single-unit recording techniques revealed that chronic cold stress significantly alters both the basal and the evoked electrophysiological activity of noradrenergic neurons in the locus coeruleus of the anaesthetized rat. Following 17-21 days of chronic cold exposure (5 degrees C), the single-unit activity of histologically-identified locus coeruleus neurons in chloral hydrate-anaesthetized rats was recorded and analysed in terms of their basal firing rate and pattern of spike activity, as well as their response to footshock stimulation. There was no significant difference in the incidence of spontaneously active cells/electrode track between cold-stressed rats and control rats. However, the basal spike activity of locus coeruleus cells recorded from cold-stressed rats differed significantly from that of control rats along two dimensions: i) they displayed significantly higher basal firing rates (mean = 1.88 Hz vs 1.20 Hz, respectively); and ii) they frequently exhibited spontaneous burst-firing activity that was not observed in control rats (observed in 15/17 cold-stressed rats vs 1/26 control rats). The evoked spike activity of locus coeruleus cells in cold-stressed rats also differed significantly from that of control rats along two dimensions: i) they were more likely to respond to footshock stimulation (mean = 90.3% vs 74.4%, respectively); and ii) these responses were more likely to consist of multispike bursts of action potentials (mean = 8 bursts/50 stimulations vs 1 burst/50 stimulations, respectively). These results indicate that alterations in the electrophysiological activity of noradrenergic locus coeruleus neurons may contribute to the phenomenon of stress-induced sensitization of norepinephrine release that is thought to underlie some of the neuropathological changes that accompany long-term stress.
体内细胞外单单位记录技术表明,慢性冷应激显著改变了麻醉大鼠蓝斑中去甲肾上腺素能神经元的基础电生理活动和诱发电生理活动。在17 - 21天的慢性冷暴露(5摄氏度)后,记录并分析了水合氯醛麻醉大鼠中经组织学鉴定的蓝斑神经元的单单位活动,包括其基础放电率、动作电位发放模式以及对足部电击刺激的反应。冷应激大鼠和对照大鼠之间自发活动细胞/电极轨迹的发生率没有显著差异。然而,冷应激大鼠记录到的蓝斑细胞基础动作电位活动在两个维度上与对照大鼠有显著差异:i)它们显示出显著更高的基础放电率(分别为平均1.88赫兹和1.20赫兹);ii)它们经常表现出对照大鼠未观察到的自发爆发式放电活动(15/17的冷应激大鼠观察到,而对照大鼠为1/26)。冷应激大鼠中蓝斑细胞的诱发动作电位活动在两个维度上也与对照大鼠有显著差异:i)它们对足部电击刺激的反应更有可能发生(分别为平均90.3%和74.4%);ii)这些反应更有可能由多个动作电位爆发组成(分别为平均8次爆发/50次刺激和1次爆发/50次刺激)。这些结果表明,去甲肾上腺素能蓝斑神经元电生理活动的改变可能促成了应激诱导的去甲肾上腺素释放敏感化现象,这被认为是长期应激伴随的一些神经病理变化的基础。