PMID- 14992289
OWN - NLM
STAT- MEDLINE
DCOM- 20040817
LR  - 20190823
IS  - 0364-3190 (Print)
IS  - 0364-3190 (Linking)
VI  - 29
IP  - 1
DP  - 2004 Jan
TI  - Glutamate-induced inhibition of D-aspartate uptake in Muller glia from the 
      retina.
PG  - 295-304
AB  - Muller glial cells from the retina "in situ" and in primary culture, mainly 
      express the high-affinity sodium-coupled glutamate/aspartate transporter GLAST-1, 
      which dominates total retinal glutamate (Glu) uptake, suggesting a major role for 
      these cells in the modulation of excitatory transmission. The possible 
      involvement of ionotropic and metabotropic Glu receptors in the regulation of Glu 
      uptake was studied in primary cultures of Muller glia. We demonstrate that 
      exposure to 1 mM L-Glu induces a time-dependent inhibition of D-aspartate (D-Asp) 
      uptake in a Na+-dependent manner, as a result of a reduction in the number of 
      transporters at the plasma membrane. The inhibition of D-Asp uptake by Glu was 
      not mimicked by agonists or modified by antagonists of ionotropic and 
      metabotropic Glu receptors. In contrast, transport was inhibited by GLAST-1 
      transportable substrates threo-hydroxyaspartate and aspartate-beta-hydroxamate, 
      but not by the nontransportable inhibitors trans-pyrrolidine dicarboxylate or 
      DL-threo-beta-benzyloxyaspartic acid. Under the same experimental conditions, 
      L-Glu did not affect the sodium-dependent transport systems for glycine or GABA. 
      The present results demonstrate that the specific downregulation of 
      glutamate/aspartate transport by L-Glu is unrelated to Glu receptor activation, 
      and results from the internalization of transporter proteins triggered by the 
      transport process itself. Such negative feedback of Glu on Glu transport, could 
      contribute to retinal toxicity under pathological conditions in which high 
      extracellular concentrations of Glu are reached.
FAU - Gadea, Ana
AU  - Gadea A
AD  - Instituto de Fisiologia Celular, Departamento de Neurociencias, UNAM, Mexico, DF, 
      Mexico.
FAU - Lopez, Edith
AU  - Lopez E
FAU - Lopez-Colome, Ana Maria
AU  - Lopez-Colome AM
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Neurochem Res
JT  - Neurochemical research
JID - 7613461
RN  - 0 (Excitatory Amino Acid Antagonists)
RN  - 0 (Receptors, Glutamate)
RN  - 3KX376GY7L (Glutamic Acid)
RN  - 4SR0Q8YD1X (D-Aspartic Acid)
SB  - IM
MH  - Animals
MH  - Cells, Cultured
MH  - Chick Embryo
MH  - D-Aspartic Acid/*metabolism
MH  - Excitatory Amino Acid Antagonists/pharmacology
MH  - Glutamic Acid/*pharmacology
MH  - Neuroglia/cytology/*drug effects/metabolism
MH  - Receptors, Glutamate/drug effects
MH  - Retina/cytology/*drug effects/metabolism
MH  - Signal Transduction
EDAT- 2004/03/03 05:00
MHDA- 2004/08/18 05:00
CRDT- 2004/03/03 05:00
PHST- 2004/03/03 05:00 [pubmed]
PHST- 2004/08/18 05:00 [medline]
PHST- 2004/03/03 05:00 [entrez]
AID - 10.1023/b:nere.0000010458.45085.e8 [doi]
PST - ppublish
SO  - Neurochem Res. 2004 Jan;29(1):295-304. doi: 10.1023/b:nere.0000010458.45085.e8.