Australian School of Advanced Medicine, Macquarie University, NSW, Australia.
Brain Res. 2012 Feb 23;1439:34-43. doi: 10.1016/j.brainres.2011.12.058. Epub 2012 Jan 5.
The tonic activity of bulbospinal neurones in the rostral ventrolateral medulla (RVLM) is thought to underlie basal sympathetic nerve activity. A key research objective is to delineate the mechanisms that contribute to the firing of these neurones. In the current study we investigate the hypothesis that inputs arising in the contralateral RVLM converge on barosensitive bulbospinal neurones and contribute to their discharge pattern. Extracellular recordings were made from 24 barosensitive bulbospinal neurones in urethane anaesthetised, vagotomised and artificially ventilated rats during activation (glutamate or D,L-homocysteic acid microinjection, 50 nl, 50mM, or monopolar electrical stimulation) or inhibition (microinjection of GABA receptor agonists muscimol or isoguvacine, 50 nl, 10mM) of the contralateral RVLM. Chemical RVLM activation strongly increased (10/17) or inhibited (6/17) the spontaneous activity of neurones recorded in the contralateral RVLM. Electrical RVLM stimulation evoked a combination of short latency (median 6 ms) inhibitory and longer latency (median 9.1 ms, P<0.01) excitatory orthodromic responses in contralateral sympathetic premotor neurones and in some cases evoked antidromic action potentials that collided with spontaneous spikes. RVLM inhibition increased the discharge rate of sympathetic premotor neurones in the contralateral brainstem by 21 ± 13% (P<0.05) and reduced the variability of unit firing by 37 ± 12% (n=5, p<0.05). These findings indicate that sympathetic premotor neurones receive inhibitory and excitatory input from the contralateral RVLM, that inhibitory inputs predominate under baseline conditions, and that a population of sympathetic premotor neurones project to the contralateral RVLM in addition to their spinal targets.
延髓头端腹外侧区（RVLM）中的紧张性神经元活动被认为是基础交感神经活动的基础。一个关键的研究目标是描绘有助于这些神经元放电的机制。在目前的研究中，我们假设来自对侧 RVLM 的传入会聚在压力敏感的球旁神经元上，并有助于它们的放电模式。在戊巴比妥钠麻醉、迷走神经切断和人工通气的大鼠中，我们在激活（谷氨酸或 D,L-同型半胱氨酸微注射，50nl，50mM，或单极电刺激）或抑制（GABA 受体激动剂 muscimol 或异古乌头碱微注射，50nl，10mM）对侧 RVLM 期间，从 24 个压力敏感的球旁神经元中进行了细胞外记录。化学 RVLM 激活强烈增加（10/17）或抑制（6/17）在对侧 RVLM 中记录的神经元的自发性活动。电 RVLM 刺激在对侧交感节前神经元中诱发了短潜伏期（中位 6ms）抑制和较长潜伏期（中位 9.1ms，P<0.01）兴奋性的传入反应，在某些情况下，还诱发了与自发性尖峰相碰撞的逆行动作电位。RVLM 抑制使对侧脑干中的交感节前神经元的放电率增加了 21±13%（P<0.05），并使单位放电的变异性降低了 37±12%（n=5，p<0.05）。这些发现表明，交感节前神经元从对侧 RVLM 接收抑制性和兴奋性输入，在基线条件下抑制性输入占主导地位，并且除了脊髓靶向外，还有一部分交感节前神经元投射到对侧 RVLM。
