PMID- 8757252
OWN - NLM
STAT- MEDLINE
DCOM- 19961125
LR  - 20191101
IS  - 0270-6474 (Print)
IS  - 1529-2401 (Electronic)
IS  - 0270-6474 (Linking)
VI  - 16
IP  - 17
DP  - 1996 Sep 1
TI  - Mechanisms of H+ and Na+ changes induced by glutamate, kainate, and D-aspartate 
      in rat hippocampal astrocytes.
PG  - 5393-404
AB  - The excitatory transmitter glutamate (Glu), and its analogs kainate (KA), and 
      D-aspartate (D-Asp) produce significant pH changes in glial cells. 
      Transmitter-induced pH changes in glial cells, generating changes in 
      extracellular pH, may represent a special form of neuronal-glial interaction. We 
      investigated the mechanisms underlying these changes in intracellular H+ 
      concentration ([H+]i) in cultured rat hippocampal astrocytes and studied their 
      correlation with increases in intracellular Na+ concentration ([Na+]i), using 
      fluorescence ratio imaging with 2',7'-bis(carboxyethyl)-5,6-carboxyfluorescein 
      (BCECF) or sodium-binding benzofuran isophthalate (SBFI). Glu, KA, or D-Asp 
      evoked increases in [Na+]i; Glu or D-Asp produced parallel acidifications. KA, in 
      contrast, evoked biphasic changes in [H+]i, alkaline followed by acid shifts, 
      which were unaltered after Ca2+ removal and persisted in 0 CI(-)-saline, but were 
      greatly reduced in CO2/HCO3(-)-free or Na(+)-free saline, or during 
      4,4'-diisothiocyanato-stilbene-2,2'-disulphonic acid (DIDS) application. The 
      non-NMDA receptor antagonist 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) blocked 
      KA-evoked changes in [H+]i and [Na+]i, indicating that they were 
      receptor-ionophore mediated. In contrast, CNQX increased the [H+]i change and 
      decreased the [Na+]i change induced by Glu. D-Asp, which is transported but does 
      not act at Glu receptors, induced [H+]i and [Na+]i changes that were virtually 
      unaltered by CNQX. Our study indicates that [Na+]i increases are not primarily 
      responsible for Glu- or KA-induced acidifications in astrocytes. Instead, 
      intracellular acidifications evoked by Glu or D-Asp are mainly caused by 
      transmembrane movement of acid equivalents associated with Glu/Asp-uptake into 
      astrocytes. KA-evoked biphasic [H+]i changes, in contrast, are probably 
      attributable to transmembrane ion movements mediated by inward, followed by 
      outward, electrogenic Na+/HCO3- cotransport, reflecting KA-induced biphasic 
      membrane potential changes.
FAU - Rose, C R
AU  - Rose CR
AD  - Department of Neurology, Yale University School of Medicine, New Haven, 
      Connecticut 06510, USA.
FAU - Ransom, B R
AU  - Ransom BR
LA  - eng
GR  - R01 NS015589/NS/NINDS NIH HHS/United States
GR  - NS-06208/NS/NINDS NIH HHS/United States
GR  - NS-15589/NS/NINDS NIH HHS/United States
PT  - Comparative Study
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - J Neurosci
JT  - The Journal of neuroscience : the official journal of the Society for 
      Neuroscience
JID - 8102140
RN  - 0 (Bicarbonates)
RN  - 0 (Buffers)
RN  - 142M471B3J (Carbon Dioxide)
RN  - 30KYC7MIAI (Aspartic Acid)
RN  - 3KX376GY7L (Glutamic Acid)
RN  - 451W47IQ8X (Sodium Chloride)
RN  - 6OTE87SCCW (6-Cyano-7-nitroquinoxaline-2,3-dione)
RN  - 7YNJ3PO35Z (Hydrogen)
RN  - 9NEZ333N27 (Sodium)
RN  - SIV03811UC (Kainic Acid)
SB  - IM
MH  - 6-Cyano-7-nitroquinoxaline-2,3-dione/pharmacology
MH  - Animals
MH  - Animals, Newborn
MH  - Aspartic Acid/pharmacology
MH  - Astrocytes/*drug effects/metabolism
MH  - Bicarbonates/metabolism
MH  - Buffers
MH  - Carbon Dioxide/physiology
MH  - Glutamic Acid/*analogs & derivatives/*pharmacology
MH  - Hippocampus/cytology/*drug effects
MH  - Hydrogen/*metabolism
MH  - Kainic Acid/pharmacology
MH  - Osmolar Concentration
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Sodium/*metabolism
MH  - Sodium Chloride/chemistry
PMC - PMC6578898
EDAT- 1996/09/01 00:00
MHDA- 1996/09/01 00:01
PMCR- 1997/03/01
CRDT- 1996/09/01 00:00
PHST- 1996/09/01 00:00 [pubmed]
PHST- 1996/09/01 00:01 [medline]
PHST- 1996/09/01 00:00 [entrez]
PHST- 1997/03/01 00:00 [pmc-release]
AID - 10.1523/JNEUROSCI.16-17-05393.1996 [doi]
PST - ppublish
SO  - J Neurosci. 1996 Sep 1;16(17):5393-404. doi: 10.1523/JNEUROSCI.16-17-05393.1996.