Increased glutamate uptake and glutamine synthetase activity in neuronal cell cultures surviving chronic hypoxia

Increased glutamate uptake and glutamine synthetase activity in neuronal cell cultures surviving... To examine the neurochemical effects of chronic hypoxia on immature nervous tissue in vitro, mixed neuronal–glial cell cultures derived from fetal mice were exposed to 5% O2 for 24 or 48 h. Those cultures subjected to longer hypoxia manifested improved neuronal survival compared to those with the shorter insult, both with respect to neuronal morphology and also cell counts. Neurochemical assays were performed on living cells in situ to determine the possible basis for differential cell survival. After both exposure conditions, Ro5–4864‐displaceable benzodiazepine (BDZ) binding, reflecting nonneuronal BDZ binding sites, was either not reduced or was elevated. Although initially reduced, binding of the excitatory amino acid (EAA) glutamate was progressively increased after both insults and, within 2 days after return to normoxia, was increased relative to control values (121 and 128% of controls, P < 0.05). The most impressive neurochemical differences between the two conditions related to changes in the predominantly or exclusively glial functions of glutamate uptake and glutamine synthetase activity. In those cultures with relatively preserved neuronal morphology: 1) high affinity uptake of glutamate was elevated compared to the shorter hypoxic insult by 3 days of recovery (104 vs 70%, P < 0.001) and 2) glutamine synthetase, an enzyme localized primarily within astrocytes, was significantly elevated even when compared to absolute control values (148%, P < 0.001). These data suggest that longer periods of hypoxia may be less deleterious to neurons than shorter hypoxic events because of a time‐dependent stimulation of specific glial cell functions which relate to increased metabolism of potentially neurotoxic EAAs such as glutamate. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Glia Wiley

Increased glutamate uptake and glutamine synthetase activity in neuronal cell cultures surviving chronic hypoxia

Glia, Volume 3 (5) – Jan 1, 1990

Loading next page...
 
/lp/wiley/increased-glutamate-uptake-and-glutamine-synthetase-activity-in-wfptj3CFLM
Publisher
Wiley
Copyright
Copyright © 1990 Wiley‐Liss, Inc.
ISSN
0894-1491
eISSN
1098-1136
D.O.I.
10.1002/glia.440030506
Publisher site
See Article on Publisher Site

Abstract

To examine the neurochemical effects of chronic hypoxia on immature nervous tissue in vitro, mixed neuronal–glial cell cultures derived from fetal mice were exposed to 5% O2 for 24 or 48 h. Those cultures subjected to longer hypoxia manifested improved neuronal survival compared to those with the shorter insult, both with respect to neuronal morphology and also cell counts. Neurochemical assays were performed on living cells in situ to determine the possible basis for differential cell survival. After both exposure conditions, Ro5–4864‐displaceable benzodiazepine (BDZ) binding, reflecting nonneuronal BDZ binding sites, was either not reduced or was elevated. Although initially reduced, binding of the excitatory amino acid (EAA) glutamate was progressively increased after both insults and, within 2 days after return to normoxia, was increased relative to control values (121 and 128% of controls, P < 0.05). The most impressive neurochemical differences between the two conditions related to changes in the predominantly or exclusively glial functions of glutamate uptake and glutamine synthetase activity. In those cultures with relatively preserved neuronal morphology: 1) high affinity uptake of glutamate was elevated compared to the shorter hypoxic insult by 3 days of recovery (104 vs 70%, P < 0.001) and 2) glutamine synthetase, an enzyme localized primarily within astrocytes, was significantly elevated even when compared to absolute control values (148%, P < 0.001). These data suggest that longer periods of hypoxia may be less deleterious to neurons than shorter hypoxic events because of a time‐dependent stimulation of specific glial cell functions which relate to increased metabolism of potentially neurotoxic EAAs such as glutamate.

Journal

GliaWiley

Published: Jan 1, 1990

References

You’re reading a free preview. Subscribe to read the entire article.


DeepDyve is your
personal research library

It’s your single place to instantly
discover and read the research
that matters to you.

Enjoy affordable access to
over 18 million articles from more than
15,000 peer-reviewed journals.

All for just $49/month

Explore the DeepDyve Library

Search

Query the DeepDyve database, plus search all of PubMed and Google Scholar seamlessly

Organize

Save any article or search result from DeepDyve, PubMed, and Google Scholar... all in one place.

Access

Get unlimited, online access to over 18 million full-text articles from more than 15,000 scientific journals.

Your journals are on DeepDyve

Read from thousands of the leading scholarly journals from SpringerNature, Elsevier, Wiley-Blackwell, Oxford University Press and more.

All the latest content is available, no embargo periods.

See the journals in your area

DeepDyve

Freelancer

DeepDyve

Pro

Price

FREE

$49/month
$360/year

Save searches from
Google Scholar,
PubMed

Create folders to
organize your research

Export folders, citations

Read DeepDyve articles

Abstract access only

Unlimited access to over
18 million full-text articles

Print

20 pages / month

PDF Discount

20% off