Neurons of a limited subthalamic area mediate elevations in cortical cerebral blood flow evoked by hypoxia and excitation of neurons of the rostral ventrolateral medulla
Neurons of a limited subthalamic area mediate elevations in cortical cerebral blood flow evoked by hypoxia and excitation of neurons of the rostral ventrolateral medulla
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DOI：
10.1523/jneurosci.21-11-04032.2001
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发表时间：
2001-06-01
影响因子：
5.3
通讯作者：
Reis, DJ
中科院分区：
文献类型：
--
作者：
Golanov, EV;Christensen, JRC;Reis, DJ
延髓头端腹外侧的交感兴奋性网状脊髓神经元（RVLM）是缺氧激发的氧探测器，可整体提高局部脑血流量（rCBF）。该投射占缺氧性脑血管舒张的 50% 以上，通过髓质血管舒张区 (MCVA) 传递。然而，RVLM/MCVA 没有直接的皮质投射，这表明有一个广泛神经支配皮质的中继，可能起源于丘脑核。通过对丘脑和底丘脑进行电微刺激进行的系统绘图显示，rCBF 的升高仅从有限区域引起，其中包括未定带内侧极、福雷尔视野和红前区。活动部位的刺激（10 秒训练）可使 rCBF 增加 25 +/- 6%。用红藻氨酸刺激局部神经元，通过增加 rCBF 来模拟电刺激的效果。用单脉冲（0.5 毫秒；80 μA）刺激丘脑底脑血管舒张区 (SVA) 会触发潜伏期为 24 +/- 5 毫秒的皮层 EEG 突发 CBF 波复合体，其形状与 MCVA 诱发的复合体相似。选择性双侧损伤 SVA 神经元（鹅膏蕈酸，2 杯，200 nl）可阻断 MCVA 引起的血管舒张，并使缺氧性脑血管舒张减弱 52 +/- 12% (p < 0.05)，而高碳酸血管舒张仍保留。基底前脑血管舒张部位的损伤未能改变 SVA 诱发的 rCBF 增加。我们得出结论：(1) 底丘脑功能受限区域的内在神经元的兴奋会升高 rCBF，(2) 这些神经元传递来自 MCVA 的信号，从而在缺氧时升高 rCBF，(3) SVA 是功能上重要的部位，将血管舒张信号从延髓传递到端脑。
Sympathoexcitatory reticulospinal neurons of the rostral ventrolateral medulla (RVLM) are oxygen detectors excited by hypoxia to globally elevate regional cerebral blood flow (rCBF). The projection, which accounts for >50% of hypoxic cerebral vasodilation, relays through the medullary vasodilator area (MCVA). However, there are no direct cortical projections from the RVLM/ MCVA, suggesting a relay that diffusely innervates cortex and possibly originates in thalamic nuclei. Systematic mapping by electrical microstimulation of the thalamus and subthalamus revealed that elevations in rCBF were elicited only from a limited area, which encompassed medial pole of zona incerta, Forel's field, and prerubral zone. Stimulation (10 sec train) at an active site increased rCBF by 25 +/- 6%. Excitation of local neurons with kainic acid mimicked effects of electrical stimulation by increasing rCBF. Stimulation of the subthalamic cerebrovasodilator area (SVA) with single pulses (0.5 msec; 80 muA) triggered cortical EEG burst-CBF wave complexes with latency 24 +/- 5 msec, which were similar in shape to complexes evoked from the MCVA. Selective bilateral lesioning of the SVA neurons (ibotenic acid, 2 mug, 200 nl) blocked the vasodilation elicited from the MCVA and attenuated hypoxic cerebrovasodilation by 52 +/- 12% ( p < 0.05), whereas hypercarbic vasodilation remained preserved. Lesioning of the vasodilator site in the basal forebrain failed to modify SVA-evoked rCBF increase. We conclude that (1) excitation of intrinsic neurons of functionally restricted region of subthalamus elevates rCBF, (2) these neurons relay signals from the MCVA, which elevate rCBF in response to hypoxia, and (3) the SVA is a functionally important site conveying vasodilator signal from the medulla to the telencephalon.