Calcium dependence of glutamate receptor-evoked alkaline shifts in hippocampus

Sabrina E. Smith; Jay A. Gottfried; Joseph C T Chen; Mitchell Chesler

doi:10.1097/00001756-199412000-00009

Calcium dependence of glutamate receptor-evoked alkaline shifts in hippocampus

Sabrina E. Smith, Jay A. Gottfried, Joseph C T Chen, Mitchell Chesler^*

^*Corresponding author for this work

Neurology

Research output: Contribution to journal › Article › peer-review

25 Scopus citations

Abstract

GLUTAMATE receptor activation induces an extracellular alkalinization in rodent hippocampus. We studied its Ca²⁺ dependence and pharmacology in hippocampal slices. Glutamate-evoked alkaline shifts were blocked by 0 Ca²⁺ saline. Alkalinizations induced by AMPA (α-amino-3-hydroxy-5-methylisoxazole-4-propionic acid) and NMDA (N-methyl-D-aspartate) were abolished by 20 μM CNQX (6-cyano-7-nitro-nitroquinoxaline-2,3-dione) and 50 μM APV (DL-2-amino-5-phosphonovaIerate), respectively. The AMPA-and NMDA-evoked alkaline shifts were blocked by 0 Ca²⁺, however, AMPA-induced [K⁺]_o elevation was unaffected. These data suggest that the glutamate receptor-channel does not mediate H⁺ influx, and support a role for Ca²⁺-H⁺ exchange.

Original language	English (US)
Pages (from-to)	2441-2445
Number of pages	5
Journal	Neuroreport
Volume	5
Issue number	18
DOIs	https://doi.org/10.1097/00001756-199412000-00009
State	Published - Dec 1994

Keywords

Ampa
Ca-H
Excitatory synaptic transmission
Extracellular pH
Glutamate
Glutamate uptake
Hippocampus
Nmda

ASJC Scopus subject areas

Neuroscience(all)

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title = "Calcium dependence of glutamate receptor-evoked alkaline shifts in hippocampus",

abstract = "GLUTAMATE receptor activation induces an extracellular alkalinization in rodent hippocampus. We studied its Ca2+ dependence and pharmacology in hippocampal slices. Glutamate-evoked alkaline shifts were blocked by 0 Ca2+ saline. Alkalinizations induced by AMPA (α-amino-3-hydroxy-5-methylisoxazole-4-propionic acid) and NMDA (N-methyl-D-aspartate) were abolished by 20 μM CNQX (6-cyano-7-nitro-nitroquinoxaline-2,3-dione) and 50 μM APV (DL-2-amino-5-phosphonovaIerate), respectively. The AMPA-and NMDA-evoked alkaline shifts were blocked by 0 Ca2+, however, AMPA-induced [K+]o elevation was unaffected. These data suggest that the glutamate receptor-channel does not mediate H+ influx, and support a role for Ca2+-H+ exchange.",

keywords = "Ampa, Ca-H, Excitatory synaptic transmission, Extracellular pH, Glutamate, Glutamate uptake, Hippocampus, Nmda",

author = "Smith, {Sabrina E.} and Gottfried, {Jay A.} and Chen, {Joseph C T} and Mitchell Chesler",

year = "1994",

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AU - Gottfried, Jay A.

AU - Chen, Joseph C T

AU - Chesler, Mitchell

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N2 - GLUTAMATE receptor activation induces an extracellular alkalinization in rodent hippocampus. We studied its Ca2+ dependence and pharmacology in hippocampal slices. Glutamate-evoked alkaline shifts were blocked by 0 Ca2+ saline. Alkalinizations induced by AMPA (α-amino-3-hydroxy-5-methylisoxazole-4-propionic acid) and NMDA (N-methyl-D-aspartate) were abolished by 20 μM CNQX (6-cyano-7-nitro-nitroquinoxaline-2,3-dione) and 50 μM APV (DL-2-amino-5-phosphonovaIerate), respectively. The AMPA-and NMDA-evoked alkaline shifts were blocked by 0 Ca2+, however, AMPA-induced [K+]o elevation was unaffected. These data suggest that the glutamate receptor-channel does not mediate H+ influx, and support a role for Ca2+-H+ exchange.

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