Regulation of excitatory transmission at hippocampal synapses by calbindin D28k.

AUTOR(ES)

Chard, P S

RESUMO

Distinct subpopulations of neurons in the brain contain one or more of the Ca(2+)-binding proteins calbindin D28k, calretinin, and parvalbumin. Although it has been shown that these high-affinity Ca(2+)-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.

Documentos Relacionados

• Nucleotide sequence of the promoter region of the gene encoding chicken calbindin D28K.
• Dynamics of dendritic calcium transients evoked by quantal release at excitatory hippocampal synapses
• Deficits in memory and hippocampal long-term potentiation in mice with reduced calbindin D28K expression.
• Expression of calbindin-D28K in motoneuron hybrid cells after retroviral infection with calbindin-D28K cDNA prevents amyotrophic lateral sclerosis IgG-mediated cytotoxicity.
• Sr2+ and quantal events at excitatory synapses between mouse hippocampal neurons in culture.