GLOBAL REDUCTION IN CEREBRAL BLOOD-FLOW AND METABOLISM ELICITED FROM INTRINSIC NEURONS OF FASTIGIAL NUCLEUS
GLOBAL REDUCTION IN CEREBRAL BLOOD-FLOW AND METABOLISM ELICITED FROM INTRINSIC NEURONS OF FASTIGIAL NUCLEUS
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DOI：
10.1016/0006-8993(89)90312-0
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发表时间：
1989-10-23
期刊：
影响因子：
2.9
通讯作者：
REIS, DJ
中科院分区：
文献类型：
--
作者：
CHIDA, K;IADECOLA, C;REIS, DJ
我们试图确定是否在区域脑血流量（rCBF）的整体增加所产生的电刺激的喙小脑顶核（FN）是一个结果的兴奋的内在神经元的FN或轴突的纤维通过或投射到it. Studies进行了麻醉与氯醛糖，麻痹和通气的大鼠。以[14 C]碘安替比林为示踪剂测定11个脑区的rCBF，以[14 C]2-脱氧葡萄糖为示踪剂测定11个脑区的局部脑葡萄糖利用率（rCGU）。FN中的神经元胞体通过局部显微注射谷氨酸类似物红藻氨酸（KA）（100 nl中5 nmol）进行化学兴奋。KA引起动脉压和心率短暂而显着的下降，即峰降压反应（FDR）。相关的是一个显着的和对称的rCBF减少，44%的控制，在所有地区，除了髓质。反应是部位和药物特异性的，与低血压无关。KA还显著地和成比例地降低了相同的10个脑区中的rCGU至对照的52%。在所有区域中，KA引起的rCBF和rCGU降低幅度呈线性相关。通过局部微量注射兴奋性毒素鹅膏蕈氨酸（IBO）（10 μ g/μ l，0.4 μ l）慢性破坏FN的内在神经元。破坏固有FN神经元对静息rCBF没有影响，也没有对电刺激FN引起的全球脑血管舒张作用。我们的结论是：（a）FN的内在神经元的兴奋引起脑代谢的广泛减少，其次是血流量的减少;（B）FN神经元不对脑血流量或代谢产生长期的紧张性影响;（c）FN的电刺激引起的rCBF的整体增加是轴突投射到或穿过核的兴奋的结果。
We sought to determine whether the global increase in regional cerebral blood flow (rCBF) produced by electrical stimulation of the rostral cerebellar fastigial nucleus (FN) is a consequence of excitation of intrinsic neurons of the FN or of axons of fibers passing through or projecting into it. Studies were conducted in rats anesthetized with chloralose, paralyzed and ventilated. rCBF was measured with [14C]iodoantipyrine as tracer and regional cerebral glucose utilization (rCGU) by [14C]2-deoxyglucose in homogenates of 11 brain regions. Neuronal perikarya in FN were excited chemically by local microinjection of the glutamate analogue kainic acid (KA) (5 nmol in 100 nl). KA elicited a transient and significant fall of arterial pressure and heart rate, the fastigial depressor response (FDR). Associated was a significant and symmetrical reduction in rCBF, to 44% of control in all regions except medulla. The response was site- and agent-specific and unrelated to the hypotension. KA also significantly and proportionally reduced, to 52% of control, rCGU in the same 10 areas of brain. In all regions the magnitudes of the reductions in rCBF and rCGU elicited by KA were linearly related. Intrinsic neurons of FN were chronically destroyed by local microinjection of the excitotoxin ibotenic acid (IBO) (10 .mu.g/.mu.l in 0.4 .mu.l). Destruction of intrinsic FN neurons had no effect on resting rCBF nor on the global cerebrovascular vasodilation elicited by electrical stimulation of the FN. We conclude that: (a) excitation of intrinsic neurons of FN elicits a widespread reduction of cerebral metabolism and, secondarily, blood flow; (b) FN neurons do not exert a long-term tonic influence on brain blood flow nor metabolism; (c) the global increase in rCBF elicited by electrical stimulation of the FN is a consequence of excitation of axons projecting into or through the nucleus.