Central Nervous System Astroglial Cells Release Nitrogen Oxide(s) with Vasorelaxant Properties

Murphy, Seán; Minor, Robert L.; Welk, Greg; Harrison, David G.

doi:10.1097/00005344-199100001-00047

Cited by 13 publications

(11 citation statements)

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“…1992). Astrocytes have also been reported as a production site for nitric oxide (Murphy et al, 1991). Our own investigations showed that cultured microglia release only little amounts of nitric oxide (Marletta et al, 1988; Griess reagent: 0.1% naphthylethylene diamine dihydrochloride, 5% H,P04, 0.1% sulfonamide; absorbance measured a t 543 nm).…”

Section: Reactive Oxygen Intermediatesmentioning

confidence: 96%

Cytotoxicity of microglia

Bánati

Gehrmann

Schubert

et al. 1993

Glia

974

271

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The most characteristic property of microglia is their swift activation in response to neuronal stress and their capacity for site-directed phagocytosis. The transformation of microglia into intrinsic brain macrophages appears to be under strict control and takes place if neuronal and/or terminal degeneration occurs in response to nerve lesion. The differentiation of microglia into brain macrophages is accompanied by the release of several secretory products, e.g., proteinases, cytokines, reactive oxygen intermediates, and reactive nitrogen intermediates. Interference with the microglial activation or the productions of cytotoxic metabolites by microglia may thus offer new therapeutic opportunities for the prevention of neuronal cell death in CNS disease.

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Section: Reactive Oxygen Intermediatesmentioning

confidence: 96%

Cytotoxicity of microglia

Bánati

Gehrmann

Schubert

et al. 1993

Glia

974

271

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“…They might thus share information of relevance for the regulation of CBF and blood brain barrier functions. The vasodilatory agent nitric oxide (NO) has recently been shown to be synthesized and released by brain astrocytes (Galea et al, 1992;Murphy et al, 1991;Simmons and Murphy, 1992) and has been suggested to have a critical role in mediating the increase in cortical CBF elicited by basal forebrain neurons (Raszkiewicz et al, 1992). Whether or not glial NO contributes to cholinergic dilatation surely deserves further investigation.…”

Section: Perivascular Astrogliamentioning

confidence: 99%

Light and electron microscopic immunocytochemical analysis of the neurovascular relationships of choline acetyltransferase and vasoactive intestinal polypeptide nerve terminals in the rat cerebral cortex

Chédotal

Umbriaco

Descarries

et al. 1994

J of Comparative Neurology

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Acetylcholine or vasoactive intestinal peptide (VIP) nerve terminals closely related to intracortical blood vessels have previously been reported. Recent physiological evidence indicates that these central neuronal systems are involved in the fine control of local cerebral blood flow. In the present study, the intimate associations between choline acetyltransferase (ChAT) and VIP axon terminals and intracortical microvessels were characterized by light (LM) and electron microscopic (EM) immunocytochemistry. In semithin sections, LM analysis of the distribution of ChAT- and VIP-immunostained puncta juxtaposed to small intraparenchymal blood vessels demonstrated that neither type of terminal was enriched or impoverished around microvessels within the cerebral cortex. At the EM level, most ChAT- or VIP-immunolabelled elements located within a 3 microns perimeter around vessel walls were axon terminals. These perivascular terminals were associated primarily with capillaries but also, to a lesser extent, with microarterioles. Even though ChAT and VIP terminals were frequently found in the immediate vicinity (< or = 0.25 microns) of microvessels, they almost never contacted the outer basal lamina, usually abutting onto perivascular astroglial leaflets. There were no membrane specializations at the site of contact between ChAT or VIP terminals and perivascular astroglia. In all cortical areas examined, the average size of VIP-immunolabelled varicosities (0.56 +/- 0.04 microns 2) was significantly larger than that of their ChAT counterparts (0.32 +/- 0.02 microns 2; P < 0.001). Perivascular VIP terminals were more frequently engaged in synaptic contact than those immunostained for ChAT, which rarely exhibited a synaptic junction even in serial thin sections. Neither VIP nor ChAT immunostaining was ever observed in endothelial cells. These results suggest that both acetylcholine and VIP exert their effects on intracortical microvessels through indirect, paracrine mechanisms. The marked difference in synaptic incidence and average size between both types of perivascular terminals indicates that these two vasoactive agents are primarily located in distinct neuronal populations. Further, our results show that the astrocytic glia is the major direct target for both ChAT and VIP perivascular terminals and suggest that neuronal/glial/vascular interactions are a key element in the neurogenic control of the intracortical microcirculation.

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“…Such activation could alter the function of astrocytic processes in contact with blood vessels in the subfornical organ (Pow and Golding, 1987;Verhage et al, 1991;Fujimoto, 1993). Enkephalin is known to produce changes in shape (Blanco et al, 1991) and/or DNA synthesis in astrocytes (O'Neill et al, 1989;Stiene-Martin and Hauser, 1990;Murphy et al, 1991;Zagon and McLaughlin, 1991). One or both of these processes could dramatically alter the relationship between neurons and vessels in the subfornical organ.…”

Section: Dense Core Vesicles and Their Relation With Astrocytesmentioning

confidence: 99%

Met⁵‐enkephalin is localized within axon terminals in the subfornical organ: Vascular contacts and interactions with neurons containing gamma‐aminobutyric acid

Pickel¹,

Chan²

1994

J of Neuroscience Research

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Met5-enkephalin inhibits sodium and water excretion and antagonizes the central actions of angiotensin II in subfornical organ of rat brain. We examined the ultrastructural basis for enkephalin modulation in this circumventricular region. Additionally, we examined the possibility that there might be cellular sites for functional interactions involving Met5-enkephalin and gamma-aminobutyric acid (GABA), a known inhibitory transmitter throughout the central nervous system. Met5-enkephalin and GABA were identified in single coronal sections through the subfornical organ using immunoperoxidase and silver-enhanced immunogold labeling methods, respectively. Enkephalin-like immunoreactivity was most prominently localized within axon terminals. These were distributed primarily in the central, highly vascular, regions of the subfornical organ. Enkephalin-labeled terminals were apposed to the basement membranes of fenestrated capillaries and also formed symmetric, inhibitory type synapses with neurons. In terminals associated with either blood vessels or neurons, the enkephalin immunoreactivity was enriched in large (80-150 nm) dense core vesicles. The immunoreactive vesicles were usually located within portions of the axon in close proximity to astrocytic processes. In contrast, smaller vesicles in the same terminals were more often aggregated near the basement membrane of the capillaries and the active zone of the synapse. The targets of enkephalin-immunoreactive terminals were either unlabeled or GABA-labeled dendrites of local neurons. Enkephalin was also co-localized with GABA in perikarya and in axon terminals. Terminals containing only GABA were far more abundant than those containing enkephalin or enkephalin and GABA. GABA-immunoreactive terminals formed symmetric synapses on unlabeled dendrites some of which also received convergent input from terminals containing enkephalin. Additionally, the enkephalin-immunoreactive terminals were closely apposed to GABA-labeled and unlabeled terminals. These results suggest sites for nonsynaptic release of Met5-enkephalin from dense core vesicles in contact with astrocytes near blood vessels and synaptic complexes in the rat subfornical organ. Moreover, the observed dual localization and pre- and postsynaptic associations between neurons containing Met5-enkephalin and GABA indicate that inhibitory effects of opioids in the subfornical organ may be mediated or potentiated by GABA.

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Central Nervous System Astroglial Cells Release Nitrogen Oxide(s) with Vasorelaxant Properties

Cited by 13 publications

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Cytotoxicity of microglia

Cytotoxicity of microglia

Light and electron microscopic immunocytochemical analysis of the neurovascular relationships of choline acetyltransferase and vasoactive intestinal polypeptide nerve terminals in the rat cerebral cortex

Met⁵‐enkephalin is localized within axon terminals in the subfornical organ: Vascular contacts and interactions with neurons containing gamma‐aminobutyric acid

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Central Nervous System Astroglial Cells Release Nitrogen Oxide(s) with Vasorelaxant Properties

Cited by 13 publications

References 0 publications

Cytotoxicity of microglia

Cytotoxicity of microglia

Light and electron microscopic immunocytochemical analysis of the neurovascular relationships of choline acetyltransferase and vasoactive intestinal polypeptide nerve terminals in the rat cerebral cortex

Met5‐enkephalin is localized within axon terminals in the subfornical organ: Vascular contacts and interactions with neurons containing gamma‐aminobutyric acid

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Met⁵‐enkephalin is localized within axon terminals in the subfornical organ: Vascular contacts and interactions with neurons containing gamma‐aminobutyric acid