GABA neurons provide a rich input to microvessels but not nitric oxide neurons in the rat cerebral cortex: A means for direct regulation of local cerebral blood flow

GABA neurons provide a rich input to microvessels but not nitric oxide neurons in the rat cerebral cortex: A means for direct regulation of local cerebral blood flow
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GABA 神经元为大鼠大脑皮层中的微血管而非一氧化氮神经元提供丰富的输入:直接调节局部脑血流的一种手段

DOI:
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发表时间:
2000
期刊:
The Journal of comparative neurology
影响因子:
--
通讯作者:
E. Hamel
E. Hamel
中科院分区:
--
文献类型:
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作者:
E. Vaucher;X. Tong;N. Cholet;Sylviane Lantin;E. Hamel

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基底前脑神经元投射到大脑皮层中的微血管和含一氧化氮(NO)合酶的神经元胞体,它们的刺激导致皮层灌注增加。γ-氨基丁酸(GABA)是这些神经元合成的第二种主要神经递质,据报道它可以改变脑微血管张力。因此,我们通过光学和电子显微镜研究了GABA神经元(标记为谷氨酸脱羧酶[GAD])与大鼠额顶叶和嗅周大脑皮质内的皮质微血管和/或NO神经元(通过烟酰胺腺嘌呤二核苷酸[NADPH-D]组织化学鉴定)的相关性。在厚切片和半薄切片上,观察到高密度的GAD斑点,数个围绕皮质内血管和神经元胞体。相比之下,NADPH-D细胞胞体和近端树突仅偶尔与GAD神经末梢接触。在超微结构水平上,血管周围和体周GAD沉积被鉴定为位于血管或未染色神经元细胞体附近或直接与血管或未染色神经元细胞体贴壁的大(0.44-0.50 μm2)神经元静脉曲张。在两个皮质区,血管周围GAD终末位于距离血管约1 μm处,并经常与相邻的神经元而不是血管成分建立连接接触(单个薄片中突触频率为25-40%)。鹅膏蕈氨酸或使君子酸毁损无名质对皮质和血管周围GAD终末的密度无明显影响,表明它们主要起源于皮质局部。这些结果表明,GABA终末可以直接与微血管床和NO神经元的胞体和近端树突是皮层GABA神经传递的主要目标。然而,基于GABA和NADPH-D在皮质神经元亚群中的共定位,我们认为这些中间神经元可能与刺激基底前脑神经元引起的皮质血管反应有关。J. Comp.神经元421:161-171,2000.© 2000 Wiley利斯公司
Basal forebrain neurons project to microvessels and the somata of nitric oxide (NO) synthase‐containing neurons in the cerebral cortex, and their stimulation results in increases in cortical perfusion. γ‐Aminobutyric acid (GABA) is the second major neurotransmitter synthesized by these neurons and it has also been reported to modify cerebromicrovascular tone. We thus investigated by light and electron microscopy the association of GABA neurons (labeled for glutamic acid decarboxylase [GAD]) with cortical microvessels and/or NO neurons (identified by nicotinamide adenine dinucleotide [NADPH‐D] histochemistry) within the frontoparietal and perirhinal cerebral cortex in the rat. On thick and semithin sections, a high density of GAD puncta was observed, several surrounded intracortical blood vessels and neuronal perikarya. In contrast, NADPH‐D cell somata and proximal dendrites were only occasionally contacted by GAD nerve terminals. Perivascular and perisomatic GAD appositions were identified at the ultrastructural level as large (0.44–0.50 μm2) neuronal varicosities located in the immediate vicinity of, or being directly apposed to, vessels or unstained neuronal cell bodies. In both cortical areas, perivascular GAD terminals were located at about 1 μm from the vessels and were seen to frequently establish junctional contacts (synaptic frequency of 25–40% in single thin sections) with adjacent neuronal but not vascular elements. Ibotenic or quisqualic acid lesion of the substantia innominata did not significantly affect the density of cortical and perivascular GAD terminals, suggesting that they mostly originated locally in the cortex. These results suggest that GABA terminals can interact directly with the microvascular bed and that the somata and proximal dendrites of NO neurons are not a major target for cortical GABA neurotransmission. However, based on the colocalization of GABA and NADPH‐D in a subset of cortical neurons, we suggest that these interneurons could be implicated in the cortical vascular response elicited by stimulation of basal forebrain neurons. J. Comp. Neurol. 421:161–171, 2000. © 2000 Wiley‐Liss, Inc.
基底前脑神经元和记忆:对鹅膏酯和使君子酯的不同易感性的生化、组织学和行为研究。
DOI: 10.1037//0735-7044.106.6.909
发表时间: 1992
影响因子: 1.9
作者:
Wenk,GL;Harrington,CA;Tucker,DA;Rance,NE;Walker,LC
通讯作者: Walker,LC