TY - JOUR
T1 - Ethanol alters glutamate but not adenosine uptake in rat astrocytes
T2 - Evidence for protein kinase C involvement
AU - Othman, Timothy
AU - Sinclair, Christopher J.D.
AU - Haughey, Norman
AU - Geiger, Jonathan D.
AU - Parkinson, Fiona E.
N1 - Funding Information:
This research was supported by the Canadian Institutes of Health Research (CIHR). TO is the recipient of a Manitoba Health Research Council (MHRC) Post-Doctoral Fellowship. FEP is a CIHR/Regional Partnerships Program Investigator. CJDS is the recipient of a studentship award from the Natural Sciences and Engineering Research Council of Canada.
Copyright:
Copyright 2017 Elsevier B.V., All rights reserved.
PY - 2002
Y1 - 2002
N2 - Glutamate is the primary excitatory neurotransmitter in brain. By stimulating neuronal activity, glutamate increases cellular energy utilization, enhances ATP hydrolysis and promotes the formation of adenosine. Adenosine has receptor-mediated effects that reduce or oppose the excitatory effects of glutamate. As a possible mechanism for ethanol's ability to inhibit excitatory effects of glutamate and enhance inhibitory effects of adenosine, we tested the hypothesis that ethanol promotes [3H]glutamate uptake and inhibits [3H]adenosine uptake. Using primary cultures of rat astrocytes, we found that acute treatment with ethanol (50 mM, 30 min) inhibited [3H]glutamate uptake and reduced protein kinase C (PKC)-induced stimulation of [3H]glutamate uptake. Prolonged treatment (50 mM, 3 day) with ethanol, however, increased both [3H]glutamate uptake and PKC activity. Contrary to other cell types, neither acute or chronic ethanol exposure affected [3H]adenosine uptake in astrocytes. These data indicate that in rat cortical astrocytes ethanol affects [3H]glutamate uptake but not [3H]adenosine uptake by affecting PKC modulation of transporter activity.
AB - Glutamate is the primary excitatory neurotransmitter in brain. By stimulating neuronal activity, glutamate increases cellular energy utilization, enhances ATP hydrolysis and promotes the formation of adenosine. Adenosine has receptor-mediated effects that reduce or oppose the excitatory effects of glutamate. As a possible mechanism for ethanol's ability to inhibit excitatory effects of glutamate and enhance inhibitory effects of adenosine, we tested the hypothesis that ethanol promotes [3H]glutamate uptake and inhibits [3H]adenosine uptake. Using primary cultures of rat astrocytes, we found that acute treatment with ethanol (50 mM, 30 min) inhibited [3H]glutamate uptake and reduced protein kinase C (PKC)-induced stimulation of [3H]glutamate uptake. Prolonged treatment (50 mM, 3 day) with ethanol, however, increased both [3H]glutamate uptake and PKC activity. Contrary to other cell types, neither acute or chronic ethanol exposure affected [3H]adenosine uptake in astrocytes. These data indicate that in rat cortical astrocytes ethanol affects [3H]glutamate uptake but not [3H]adenosine uptake by affecting PKC modulation of transporter activity.
KW - Adenosine
KW - Astrocytes
KW - Ethanol
KW - Glutamate transporters
KW - Nucleoside transporters
KW - Protein kinase C
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U2 - 10.1023/A:1014955111742
DO - 10.1023/A:1014955111742
M3 - Article
C2 - 11958530
AN - SCOPUS:0036209061
SN - 0364-3190
VL - 27
SP - 289
EP - 296
JO - Neurochemical Research
JF - Neurochemical Research
IS - 4
M1 - 373358
ER -