Purine nucleoside phosphorylase: a histochemical marker for glial cells

Reempts, J. Van; Deuren, Bruno Van; Haseldonckx, Marc; Ven, Mies Van de; Thoné, Fred; Borgers, M.

doi:10.1016/0006-8993(88)90596-3

Cited by 23 publications

(19 citation statements)

References 7 publications

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“…Hypoxanthine is in turn degraded to xanthine and uric acid by another enzyme, xanthine oxidase. The finding that PNP in rat brain is present in astrocytes and endothelial cells, but not in neurons [Van Reempts et al, 1988] suggests that the final stages of purine metabolism in the brain may take place in nonneuronal cells. Inhibition of PNP with topically applied 8-amino-9-(2-thienylmethyl) guanine (PD117,229) [Gilbertsen et al, 1987] significantly elevated cortical superfusates levels of adenosine and inosine.…”

Section: Extracellular Levels Of Adenosine and Its Metabolitesmentioning

confidence: 89%

In vivo studies of the release of adenine 5′‐nucleotides, adenosine, and its metabolites from the rat brain

Phillis

O’Regan

2003

Drug Development Research

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Adenosine 5 0 -triphosphate (ATP) and adenosine function as an excitatory neurotransmitter and a neuromodulator, respectively, in the central nervous system. Neuroexcitatory effects of ATP are mediated by P2X receptors: neuromodulator effects of adenosine by A 1 , A 2 , or A 3 receptors. There is also evidence that ATP, acting a P2Y receptor, is involved in osmoregulatory responses to cell swelling. Studies on the release of ATP and/or adenosine into the interstitial fluid of the brain have served to clarify their roles in cerebral function. ATP release occurs during electrical or K + -induced depolarization of cerebral tissues. Released ATP is rapidly hydrolyzed by ectonucleotidases, which may be released concurrently, to form adenosine 5 0 -diphosphate (ADP) and adenine 5 0 -monophosphate (AMP). In addition to synaptic release from neurons, there is evidence of glial release via gap-junction hemichannels. Hydrolysis of AMP to adenosine initiates a further metabolic cascade with the formation of inosine, hypoxanthine, xanthine, and uric acid by adenosine deaminase, purine nucleoside phosphorylase, and xanthine oxidase. Hypoxanthine can be converted to inosine monophosphate by hypoxanthine phosphoribosyl transferase and thus used to replenish ATP. Cerebral ischemia causes ATP utilization, and adenosine formation. Adenosine can then be transported across the plasma membrane and released into the interstitial space. Hypoxemia-evoked adenosine release from the cerebral cortex is inhibited by blockers of adenosine transport. Inhibition of purine metabolism by blockers of adenosine deaminase, purine nucleoside phosphorylase, and xanthine oxidase elevates upstream levels of adenosine and its metabolites. Exposure of the in vivo rat cerebral cortex to cerebrospinal fluid containing swelling-inducing monocarboxylic acids elevated interstitial fluid levels of ADP and AMP, but not of adenosine. Taken together, these studies have led to a greater understanding of the metabolism and release of adenosine and the adenine nucleotides in the normoxic and ischemic brain. Drug Dev. Res.

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Section: Extracellular Levels Of Adenosine and Its Metabolitesmentioning

confidence: 89%

In vivo studies of the release of adenine 5′‐nucleotides, adenosine, and its metabolites from the rat brain

Phillis

O’Regan

2003

Drug Development Research

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“…Scale bar in A, 10 pm; in B, 15 pm; and in C, 20 pm. The PNP-histochemistry revealed previously reported glial distribution patterns (Van Reempts et al, 1988). Quantification of the number of GFAP-and PNP-labeled astrocytes counted in adjacent sections through identical cortical profiles revealed 5022 PNP-labeled astrocytes versus 1036 GFAP-positive astrocytes.…”

Section: Percentage Of Reactive Astrocytesmentioning

confidence: 96%

Muscarinic acetylcholine receptor‐expression in astrocytes in the cortex of young and aged rats

Zee

Jong

Strosberg

et al. 1993

Glia

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The present report describes the cellular and subcellular distribution pattern of immunoreactivity to M35, a monoclonal antibody raised against purified muscarinic acetylcholine receptor protein, in astrocytes in the cerebral cortex of young and aged rats. Most M35-positive astrocytes were localized in the superficial layers of the cortex and part of the corpus callosum. At the ultrastructural level, immunoprecipitates were localized in the Golgi complexes, but the nucleus, rough endoplasmic reticulum, mitochondria, and microfilaments were generally free of labeling. Labeling was also present associated to the cell membrane, although without the characteristic immunoreactive postsynaptic membrane thickening found in neuronal structures. In aging rats of 30-34 months, the number of M35-labeled astrocytes doubled, whereas the neuronal staining slightly decreased in the same region in half of the animals studied. Fluorescent double-labeling for M35 and GFAP, an astrocytic microfilament protein, revealed that all M35-positive glial cells express GFAP and, conversely, that almost all GFAP glial cells were M35-immunostained. Based on the high incidence of coexpression of mAChRs and GFAP, both proteins may be functionally linked to each other. Rough semiquantitative estimates revealed that in young adult rats the GFAP/M35-immunoreactive astrocytes made up approximately one fifth of all cortical astrocytes. An important aspect of the presently demonstrated immunoreactivity of astroglia to mAChR proteins is its labeling in situ instead of in tissue culture. This finding may further support investigation, e.g., on anatomical relations of astroglia with neuronal and vascular elements, and its reactivity in experimental conditions.

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“…Purine nucleoside phosphorylase activity in 100-)u,m-thick coronal sections through the thalamus served as a histochemical marker for reactive gliosis in thalamic nuclei. 35 By means of digital densitometry, the difference between ipsilateral (infarct-induced) and contralateral (background) integrated density in the nucleus ventralis posterolateralis thalami was computed.…”

mentioning

confidence: 99%

Photochemical stroke model: flunarizine prevents sensorimotor deficits after neocortical infarcts in rats.

Ryck

Reempts

Borgers

et al. 1989

Stroke

323

155

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We produced unilateral photochemical infarcts in the hindlimb sensorimotor neocortex of 186 rats by intravenous injection of the fluoroscein derivative rose bengal and focal illumination of the intact skull surface. Infarcted rats showed specific, long-lasting deficits in tactile and proprioceptive placing reactions of the contralateral limbs, mostly the hindlimb. Placing deficits were most prominent during transition to immobility and/or when independent limb movements were required. Administration of flunarizine, a Class FV calcium antagonist, 30 minutes after infarction resulted in marked sparing of sensorimotor function in 30 rats. In contrast to 20 vehicle-treated rats, which remained deficient for at least 21 days, 15 (75%) of the rats treated with 1.25 mg/kg i.v. flunarizine showed normal placing on Day 1 after infarction, whereas the remaining five (25%) recovered within 5 days. Oral treatment of 10 rats with 40 mg/kg flunarizine was also effective. Neocortical infarct volume and thalamic gliosis, assessed 21 days after infarction, did not differ between 30 flunarizine-and 30 vehicle-treated rats. However, when 4-hour-old infarcts were measured in 16 rats, posttreatment with intravenous flunarizine reduced infarct size by 31%. In combination with appropriate behavioral analyses, photochemical thrombosis may constitute a relevant stroke model, in which flunarizine preserved behavioral function during a critical period, corresponding to the spread of ischemic damage. {Stroke 1989;20:1383-1390) W hen the fluorescein derivative rose bengal is intravenously injected into rats and the intact skull surface is focally illuminated, cerebral blood vessels in a confined area sustain photochemical injury. Singlet oxygen molecules generated by the dye/light interaction cause peroxidation of endothelial cell membranes and occlusive platelet aggregation. Subsequent thrombus formation, vascular stasis, extravasation, and cytotoxic edema lead to cerebral infarction and necrosis. 1-2 This photochemical model of thrombotic stroke is virtually noninvasive, allows for reproducible infarct size and location, and includes endothelial damage/platelet aggregation interactions in a cascade of stroke-like ischemic events. In this model, the time course of changes in cerebral

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Purine nucleoside phosphorylase: a histochemical marker for glial cells

Cited by 23 publications

References 7 publications

In vivo studies of the release of adenine 5′‐nucleotides, adenosine, and its metabolites from the rat brain

In vivo studies of the release of adenine 5′‐nucleotides, adenosine, and its metabolites from the rat brain

Muscarinic acetylcholine receptor‐expression in astrocytes in the cortex of young and aged rats

Photochemical stroke model: flunarizine prevents sensorimotor deficits after neocortical infarcts in rats.

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