Source of extracellular brain adenosine during hypoxia in fetal sheep

Brian J. Koos; Lawrence Kruger; Thomas F. Murray

doi:10.1016/S0006-8993(97)01207-9

Source of extracellular brain adenosine during hypoxia in fetal sheep

Brian J. Koos, Lawrence Kruger, Thomas F. Murray

Research output: Contribution to journal › Article › peer-review

33 Scopus citations

Abstract

Microdialysis was performed to determine whether hypoxia increases fetal brain adenosine (ADO) concentration through dephosphorylation of extracellular 5'-adenosine monophosphate (5-AMP). Hypoxia (fetal PaO₂ ≃ 14 Torr) increased fetal brain ADO levels ~ two-fold when the probes were perfused with synthetic cerebrospinal fluid (CSF) containing inhibitors of the nucleoside transporter but not with this solution plus a blocker of ecto- 5'-nucleotidase (AOPCP). The hypoxia-induced rise in fetal brain ADO concentrations depends critically upon the hydrolysis of extracellular 5'- AMP.

Original language	English (US)
Pages (from-to)	439-442
Number of pages	4
Journal	Brain Research
Volume	778
Issue number	2
DOIs	https://doi.org/10.1016/S0006-8993(97)01207-9
State	Published - Dec 19 1997
Externally published	Yes

All Science Journal Classification (ASJC) codes

Neuroscience(all)
Molecular Biology
Clinical Neurology
Developmental Biology

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10.1016/S0006-8993(97)01207-9

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title = "Source of extracellular brain adenosine during hypoxia in fetal sheep",

abstract = "Microdialysis was performed to determine whether hypoxia increases fetal brain adenosine (ADO) concentration through dephosphorylation of extracellular 5'-adenosine monophosphate (5-AMP). Hypoxia (fetal PaO2 ≃ 14 Torr) increased fetal brain ADO levels ~ two-fold when the probes were perfused with synthetic cerebrospinal fluid (CSF) containing inhibitors of the nucleoside transporter but not with this solution plus a blocker of ecto- 5'-nucleotidase (AOPCP). The hypoxia-induced rise in fetal brain ADO concentrations depends critically upon the hydrolysis of extracellular 5'- AMP.",

author = "Koos, {Brian J.} and Lawrence Kruger and Murray, {Thomas F.}",

note = "Funding Information: We thank Leland Patron and Judith Halle for assistance with this study. This study was supported in part by National Institute of Child Health and Human Development (NICHD) Grant HD-18478, Institute of Neurological Disorders and Stroke (NINDS) Grant NS-5685, and National Institute of Drug Abuse(NIDA) Grant DA-00217.",

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T1 - Source of extracellular brain adenosine during hypoxia in fetal sheep

AU - Koos, Brian J.

AU - Kruger, Lawrence

AU - Murray, Thomas F.

N1 - Funding Information: We thank Leland Patron and Judith Halle for assistance with this study. This study was supported in part by National Institute of Child Health and Human Development (NICHD) Grant HD-18478, Institute of Neurological Disorders and Stroke (NINDS) Grant NS-5685, and National Institute of Drug Abuse(NIDA) Grant DA-00217.

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N2 - Microdialysis was performed to determine whether hypoxia increases fetal brain adenosine (ADO) concentration through dephosphorylation of extracellular 5'-adenosine monophosphate (5-AMP). Hypoxia (fetal PaO2 ≃ 14 Torr) increased fetal brain ADO levels ~ two-fold when the probes were perfused with synthetic cerebrospinal fluid (CSF) containing inhibitors of the nucleoside transporter but not with this solution plus a blocker of ecto- 5'-nucleotidase (AOPCP). The hypoxia-induced rise in fetal brain ADO concentrations depends critically upon the hydrolysis of extracellular 5'- AMP.

AB - Microdialysis was performed to determine whether hypoxia increases fetal brain adenosine (ADO) concentration through dephosphorylation of extracellular 5'-adenosine monophosphate (5-AMP). Hypoxia (fetal PaO2 ≃ 14 Torr) increased fetal brain ADO levels ~ two-fold when the probes were perfused with synthetic cerebrospinal fluid (CSF) containing inhibitors of the nucleoside transporter but not with this solution plus a blocker of ecto- 5'-nucleotidase (AOPCP). The hypoxia-induced rise in fetal brain ADO concentrations depends critically upon the hydrolysis of extracellular 5'- AMP.

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