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A high GluR1 : GluR2 expression ratio is correlated with expression of Ca 2+ ‐binding proteins in rat forebrain neurons

A high GluR1 : GluR2 expression ratio is correlated with expression of Ca 2+ ‐binding proteins in... α‐Amino‐3‐hydroxy‐5‐methyl‐4‐isoxazle propionic acid (AMPA) receptors are ubiquitously expressed; however, their subtypes and abundance vary from region to region. We classified the neurons in various forebrain regions (hippocampus, striatum, amygdala, piriform cortex and somatosensory cortex) into six types: (R1+/R2+), (R1–/R2+), (R1+/R2–), (R1–/R2–), (R1++/R2+) and (R1++/R2–), and analysed the expression of Ca2+‐binding proteins, such as parvalbumin and calbindin‐D28k, using a triple‐staining method. The neurons showing a high GluR1 : GluR2 expression ratio, (R1+/R2–), (R1++/R2+) and (R1++/R2–) neurons, comprised 13–30% of the total neuronal population. In addition, the expression of Ca2+‐binding proteins was mainly observed in these three types of neurons. The results suggest that Ca2+‐binding protein‐positive neurons express Ca2+‐permeable AMPA receptors, because the Ca2+‐permeability of AMPA receptors is enhanced by the relative scarcity of the GluR2 subunit. To directly test the possibility that Ca2+‐binding protein‐positive neurons express Ca2+‐permeable AMPA receptors, we performed Ca2+‐imaging experiments in cultured cortical neurons. Ca2+ influx through AMPA receptors was measured selectively by addition of AMPA together with cyclothiazide in the presence of blockers of other Ca2+ influx routes. More than half of the calbindin‐D28k‐positive neurons showed a large increase in the intracellular Ca2+ concentration ((Ca2+)i), whilst most of the calbindin‐D28k‐undetectable neurons exhibited only a slight rise in (Ca2+)i after AMPA addition. These results suggest that the expression of calbindin‐D28k is related to the expression of Ca2+‐permeable AMPA receptors. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png European Journal of Neuroscience Wiley

A high GluR1 : GluR2 expression ratio is correlated with expression of Ca 2+ ‐binding proteins in rat forebrain neurons

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References (50)

Publisher
Wiley
Copyright
Copyright © 2000 Wiley Subscription Services, Inc., A Wiley Company
ISSN
0953-816X
eISSN
1460-9568
DOI
10.1046/j.1460-9568.2000.00167.x
Publisher site
See Article on Publisher Site

Abstract

α‐Amino‐3‐hydroxy‐5‐methyl‐4‐isoxazle propionic acid (AMPA) receptors are ubiquitously expressed; however, their subtypes and abundance vary from region to region. We classified the neurons in various forebrain regions (hippocampus, striatum, amygdala, piriform cortex and somatosensory cortex) into six types: (R1+/R2+), (R1–/R2+), (R1+/R2–), (R1–/R2–), (R1++/R2+) and (R1++/R2–), and analysed the expression of Ca2+‐binding proteins, such as parvalbumin and calbindin‐D28k, using a triple‐staining method. The neurons showing a high GluR1 : GluR2 expression ratio, (R1+/R2–), (R1++/R2+) and (R1++/R2–) neurons, comprised 13–30% of the total neuronal population. In addition, the expression of Ca2+‐binding proteins was mainly observed in these three types of neurons. The results suggest that Ca2+‐binding protein‐positive neurons express Ca2+‐permeable AMPA receptors, because the Ca2+‐permeability of AMPA receptors is enhanced by the relative scarcity of the GluR2 subunit. To directly test the possibility that Ca2+‐binding protein‐positive neurons express Ca2+‐permeable AMPA receptors, we performed Ca2+‐imaging experiments in cultured cortical neurons. Ca2+ influx through AMPA receptors was measured selectively by addition of AMPA together with cyclothiazide in the presence of blockers of other Ca2+ influx routes. More than half of the calbindin‐D28k‐positive neurons showed a large increase in the intracellular Ca2+ concentration ((Ca2+)i), whilst most of the calbindin‐D28k‐undetectable neurons exhibited only a slight rise in (Ca2+)i after AMPA addition. These results suggest that the expression of calbindin‐D28k is related to the expression of Ca2+‐permeable AMPA receptors.

Journal

European Journal of NeuroscienceWiley

Published: Aug 1, 2000

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