Format

Send to

Choose Destination
Mol Pain. 2017 Jan-Dec;13:1744806917719847. doi: 10.1177/1744806917719847.

Characterization of postsynaptic calcium signals in the pyramidal neurons of anterior cingulate cortex.

Author information

1
1 Center for Neuron and Disease, Frontier Institutes of Science and Technology, Xi'an Jiaotong University, Xi'an, China.
2
2 Department of Anatomy, K.K. Leung Brain Research Center, Fourth Military Medical University, Xi'an, China.
3
3 Department of Physiology, Faculty of Medicine, University of Toronto, Toronto, ON, Canada.

Abstract

Calcium signaling is critical for synaptic transmission and plasticity. N-methyl-D-aspartic acid (NMDA) receptors play a key role in synaptic potentiation in the anterior cingulate cortex. Most previous studies of calcium signaling focus on hippocampal neurons, little is known about the activity-induced calcium signals in the anterior cingulate cortex. In the present study, we show that NMDA receptor-mediated postsynaptic calcium signals induced by different synaptic stimulation in anterior cingulate cortex pyramidal neurons. Single and multi-action potentials evoked significant suprathreshold Ca2+ increases in somas and spines. Both NMDA receptors and voltage-gated calcium channels contributed to this increase. Postsynaptic Ca2+signals were induced by puff-application of glutamate, and a NMDA receptor antagonist AP5 blocked these signals in both somas and spines. Finally, long-term potentiation inducing protocols triggered postsynaptic Ca2+ influx, and these influx were NMDA receptor dependent. Our results provide the first study of calcium signals in the anterior cingulate cortex and demonstrate that NMDA receptors play important roles in postsynaptic calcium signals in anterior cingulate cortex pyramidal neurons.

KEYWORDS:

NMDA receptors; Synaptic plasticity; anterior cingulate cortex; calcium imaging; long-term potentiation; two-photon microscopy

PMID:
28726541
PMCID:
PMC5524231
DOI:
10.1177/1744806917719847
[Indexed for MEDLINE]
Free PMC Article

Supplemental Content

Full text links

Icon for Atypon Icon for PubMed Central
Loading ...
Support Center