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

Access to Document

10.1016/S0006-8993(97)01207-9

Fingerprint Dive into the research topics of 'Source of extracellular brain adenosine during hypoxia in fetal sheep'. Together they form a unique fingerprint.

Cite this

@article{0d67c28c6d8c41d38a92144e26b1ae14,

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.",

year = "1997",

month = dec,

day = "19",

doi = "10.1016/S0006-8993(97)01207-9",

language = "English (US)",

volume = "778",

pages = "439--442",

journal = "Brain Research",

issn = "0006-8993",

publisher = "Elsevier",

number = "2",

}

TY - JOUR

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.

PY - 1997/12/19

Y1 - 1997/12/19

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.

UR - http://www.scopus.com/inward/record.url?scp=0031578865&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0031578865&partnerID=8YFLogxK

U2 - 10.1016/S0006-8993(97)01207-9

DO - 10.1016/S0006-8993(97)01207-9

M3 - Article

C2 - 9459565

AN - SCOPUS:0031578865

VL - 778

SP - 439

EP - 442

JO - Brain Research

JF - Brain Research

SN - 0006-8993

IS - 2

ER -

Source of extracellular brain adenosine during hypoxia in fetal sheep

Abstract

All Science Journal Classification (ASJC) codes

Access to Document

Other files and links

Cite this