Inhibition of dendritic calcium influx by activation of G-protein-coupled receptors in the hippocampus

被引:16
作者
Chen, HM
Lambert, NA [1 ]
机构
[1] Med Coll Georgia, Dept Pharmacol & Toxicol, Augusta, GA 30912 USA
[2] Vet Affairs Med Ctr, Augusta, GA 30912 USA
关键词
D O I
10.1152/jn.1997.78.6.3484
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
G(i) proteins inhibit voltage-gated calcium channels and activate inwardly rectifying K+ channels in hippocampal pyramidal neurons. The effect of activation of G-protein-coupled receptors on action potential-evoked calcium influx was examined in pyramidal neuron dendrites with optical and extracellular voltage recording. We tested the hypotheses that 1) activation of these receptors would inhibit calcium channels in dendrites; 2) hyperpolarization resulting from K+ channel activation would deinactivate low-threshold, T-type calcium channels on dendrites, increasing calcium influx mediated by these channels; and 3) activation of these receptors would inhibit propagation of action potentials into dendrites, and thus indirectly decrease calcium influx. Activation of adenosine receptors, which couple to G(i) proteins, inhibited calcium influx in cell bodies and proximal dendrites without inhibiting action-potential propagation into the proximal dendrites. Inhibition of dendritic calcium influx was not changed in the presence of 50 mu M nickel, which preferentially blocks T-type channels, suggesting influx through these channels is not increased by activation of G-proteins. Adenosine inhibited propagation of action potentials into the distal branches of pyramidal neuron dendrites, leading to a three-to fourfold greater inhibition of calcium influx in the distal dendrites than in the soma or proximal dendrites. These results suggest that voltage-coated calcium channels are inhibited in pyramidal neuron dendrites, as they are in cell bodies and terminals and that G-protein-mediated inhibition of action-potential propagation can contribute substantially to inhibition of dendritic calcium influx.
引用
收藏
页码:3484 / 3488
页数:5
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