Dendritic spine heterogeneity and calcium dynamics in basolateral amygdala principal neurons

Power, John M. and Sah, Pankaj P. (2014) Dendritic spine heterogeneity and calcium dynamics in basolateral amygdala principal neurons. Journal of Neurophysiology, 112 7: 1616-1627. doi:10.1152/jn.00770.2013


Author Power, John M.
Sah, Pankaj P.
Title Dendritic spine heterogeneity and calcium dynamics in basolateral amygdala principal neurons
Journal name Journal of Neurophysiology   Check publisher's open access policy
ISSN 0022-3077
1522-1598
Publication date 2014-10-01
Year available 2014
Sub-type Article (original research)
DOI 10.1152/jn.00770.2013
Open Access Status
Volume 112
Issue 7
Start page 1616
End page 1627
Total pages 12
Place of publication Bethesda, MD, United States
Publisher American Physiological Society
Collection year 2015
Language eng
Abstract Glutamatergic synapses on pyramidal neurons are formed on dendritic spines where glutamate activates ionotropic receptors, and calcium influx via N-methyl-d-aspartate receptors leads to a localized rise in spine calcium that is critical for the induction of synaptic plasticity. In the basolateral amygdala, activation of metabotropic receptors is also required for synaptic plasticity and amygdala-dependent learning. Here, using acute brain slices from rats, we show that, in basolateral amygdala principal neurons, high-frequency synaptic stimulation activates metabotropic glutamate receptors and raises spine calcium by releasing calcium from inositol trisphosphate-sensitive calcium stores. This spine calcium release is unevenly distributed, being present in proximal spines, but largely absent in more distal spines. Activation of metabotropic receptors also generated calcium waves that differentially invaded spines as they propagated toward the soma. Dendritic wave invasion was dependent on diffusional coupling between the spine and parent dendrite which was determined by spine neck length, with waves preferentially invading spines with short necks. Spine calcium is a critical trigger for the induction of synaptic plasticity, and our findings suggest that calcium release from inositol trisphosphate-sensitive calcium stores may modulate homosynaptic plasticity through store-release in the spine head, and heterosynaptic plasticity of unstimulated inputs via dendritic calcium wave invasion of the spine head.
Keyword Memory
Plasticity
Metabotropic glutamate receptors
Calcium
LTD
Q-Index Code C1
Q-Index Status Confirmed Code
Institutional Status UQ

Document type: Journal Article
Sub-type: Article (original research)
Collections: Queensland Brain Institute Publications
Official 2015 Collection
 
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