Regulation of excitatory transmission at hippocampal synapses by calbindin D28k

Paul S. Chard, Joaquín Jordán, Charles J. Marcuccilli, Richard J. Miller*, Jeffrey M. Leiden, Raymond P. Roos, Ghanashyam D. Ghadge

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

104 Scopus citations

Abstract

Distinct subpopulations of neurons in the brain contain one or more of the Ca2+-binding proteins calbindin D28k. calretinin, and parvalbumin. Although it has been shown that these high-affinity Ca2+-binding proteins can increase neuronal Ca2+ buffering capacity, it is not clear which aspects of neuronal physiology they normally regulate. To investigate this problem, we used a recently developed method for expressing calbindin D28k in the somatic and synaptic regions of cultured hippocampal pyramidal neurons. Ninety-six hours after infection with a replication-defective adenovirus containing the calbindin D28k gene, essentially all cultured hippocampal pyramidal neurons robustly expressed calbindin D28k. Our results demonstrate that while calbindin D28k does not alter evoked neurotransmitter release at excitatory pyramidal cell synapses, this protein has a profound effect on synaptic plasticity. In particular, we show that calbindin D28k expression suppresses posttetanic potentiation.

Original languageEnglish (US)
Pages (from-to)5144-5148
Number of pages5
JournalProceedings of the National Academy of Sciences of the United States of America
Volume92
Issue number11
DOIs
StatePublished - May 23 1995

Keywords

  • Adenovirus
  • Calcium
  • Synaptic plasticity

ASJC Scopus subject areas

  • General

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