Extranuclear dendrites of locus coeruleus neurons: Activation by glutamate and modulation of activity by alpha adrenoceptors
Extranuclear dendrites of locus coeruleus neurons: Activation by glutamate and modulation of activity by alpha adrenoceptors
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DOI：
10.1152/jn.1995.74.6.2427
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发表时间：
1995-12-01
影响因子：
2.5
通讯作者：
AstonJones, G
中科院分区：
文献类型：
--
作者：
Ivanov, A;AstonJones, G
1.在大鼠脑片上记录到蓝斑(LC)神经元的胞外和胞内。观察谷氨酸作用于远端核外LC树突区和α-2肾上腺素能受体对这些细胞活性的影响。2.谷氨酸作用于远端树突区可有效激活LC神经元。这些反应不能被1 mM河豚毒素或2 mM CO2+-10 mM镁离子阻断。这表明谷氨酸直接作用于远端树突可以有效地激活LC神经元。α-2肾上腺素受体拮抗剂育亨宾(1mU M)或咪唑克生(1mU M)可显著增强树突状谷氨酸引起的LC神经元反应。这些拮抗剂处理也使LC神经元的自发放电活动一过性降低，而后又增加。阻断α-2肾上腺素受体后，利血平大鼠LC神经元的自发活动和谷氨酸诱发活动未见改变。这表明在非利血平的脑片中，α-2拮抗剂治疗后LC活性和对谷氨酸的反应性的改变是通过阻断内源性释放的去甲肾上腺素的作用来实现的。α-1拮抗剂哌唑嗪(1mU-M)可引起LC神经元自发放电频率的轻微但可靠的下降。在哌唑嗪预处理后，α-2拮抗剂没有引起预期的LC自发放电和对谷氨酸的反应的延迟性增加。这些结果表明，α-1肾上腺素能受体的激活可能是给予α-2拮抗剂后LC神经元兴奋性迟发性增加的原因之一。讨论了α-1和α-2肾上腺素受体在调节LC神经元自发放电频率和谷氨酸诱发反应中的可能作用。
1. Locus coeruleus (LC) neurons were recorded extracellularly and intracellularly in rat brain slices. Effects of glutamate applied to the area of distal extranuclear LC dendrites, and of alpha-2 adrenoceptors applied in the bath, were determined on activity of these cells. 2. Glutamate applied to the area of distal dendrites potently activated LC neurons. These responses were not blocked by either 1 mu M tetrodotoxin or2 mM Co2+ -10 mM Mg2+. This indicates that glutamate acting directly on distal dendrites can potently activate LC neurons.3. Bath application of the alpha-2 adrenoceptor antagonists yohimbine (1 mu M) or idazoxan (1 mu M) significantly increased responses of LC neurons evoked by dendritic glutamate application. These antagonist treatments also transiently decreased, and then increased, spontaneous discharge activity in LC neurons.4. Alterations in spontaneous and glutamate-evoked activities after blockade of alpha-2 adrenoreceptors were not observed in LC neurons of reserpinized rats. This indicates that the altered LC activity and responsiveness to glutamate following alpha-2 antagonist treatment in nonreserpinized slices are mediated via blockade of effects of endogenously released noradrenaline.5. The alpha-1 antagonist prazosin (1 mu M) caused a small but reliable decrease in the spontaneous firing rate of LC neurons. After prazosin pretreatment, alpha-2 antagonists did not evoke the expected delayed increase in LC spontaneous firing and response to glutamate application. These results indicate that activation of alpha-1 adrenoceptors may contribute to the delayed increase in excitability of LC neurons after alpha-2 antagonist administration. The possible roles of alpha-1 and alpha-2 adrenoreceptors in regulation of spontaneous discharge rate and glutamate-evoked responses in LC neurons are discussed.