School of Medical Sciences, University of New South Wales, NSW 2052, Australia.
Neuroscience. 2010 Apr 14;166(4):1210-8. doi: 10.1016/j.neuroscience.2010.01.039. Epub 2010 Jan 28.
The aim of this study was to test a possible role of A5 neurons in the expression of the pressor and tachycardic responses to conditioned fear and restraint, two forms of psychological stress. Previous Fos studies have shown that the C1 adrenergic neurons and spinally projecting neurons in the vasopressor region of the rostral ventrolateral medulla are not activated by these two stressors, suggesting that these cardiovascular changes may be mediated by other premotor sympathetic (presympathetic) cell groups. The same studies also revealed that the A5 noradrenergic group was one of the main presympathetic cell groups to be activated in response to these two stressors. Thus, we hypothesized that the A5 group could mediate these cardiovascular responses. Conditioned fear and restraint were tested in rats implanted with radiotelemetric probes before and after retrograde lesion with the selective toxin anti-dopamine-beta-hydroxylase-saporin bilaterally injected in the spinal cord at T2-T3. Six animals were selected that had the most extensive loss of spinally projecting catecholaminergic neurons: A5 (81%-95%) and rostral C1 (59%-86%, which would include most C1 bulbospinal neurons). However, despite this major loss of noradrenergic and adrenergic presympathetic neurons, the magnitude of the cardiovascular response to conditioned fear and restraint was the same before and after the lesion. Associated behavioural changes were not affected either. The results indicate that A5 presympathetic neurons are not essential for the expression of the tachycardic and pressor responses to conditioned fear and restraint. They also confirm that C1 bulbospinal neurons are not involved in these responses. The presympathetic neurons driving the tachycardic and pressor responses to conditioned fear and restraint must be elsewhere.
这项研究的目的是检验 A5 神经元在表达加压和心动过速反应中的可能作用，加压和心动过速反应是条件性恐惧和束缚这两种心理应激的形式。先前的 Fos 研究表明，C1 肾上腺素能神经元和投射到延髓腹外侧头端加压区的脊髓神经元不会被这两种应激激活，这表明这些心血管变化可能是由其他前运动性交感（预交感）细胞群介导的。同样的研究还表明，A5 去甲肾上腺素能神经元群是对这两种应激反应中被激活的主要预交感细胞群之一。因此，我们假设 A5 神经元群可以介导这些心血管反应。在双侧 T2-T3 脊髓注射选择性毒素抗多巴胺-β-羟化酶-相思豆蛋白进行逆行损伤之前和之后，对植入无线电遥测探头的大鼠进行条件性恐惧和束缚测试。选择了 6 只动物进行测试，它们的脊髓投射儿茶酚胺能神经元损失最广泛：A5（81%-95%）和头端 C1（59%-86%，其中包括大多数 C1 球脊髓神经元）。然而，尽管去甲肾上腺素能和肾上腺素能预交感神经元大量丢失，条件性恐惧和束缚引起的心血管反应的幅度在损伤前后是相同的。相关的行为变化也没有受到影响。结果表明，A5 预交感神经元对于条件性恐惧和束缚引起的心动过速和加压反应的表达不是必需的。它们还证实 C1 球脊髓神经元不参与这些反应。驱动条件性恐惧和束缚引起的心动过速和加压反应的预交感神经元一定在其他地方。
