Linked Life Data

19074019

Source:http://linkedlifedata.com/resource/pubmed/id/19074019

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
50
pubmed:dateCreated
2008-12-16
pubmed:abstractText
Dendritic spines have been proposed to function as electrical compartments for the active processing of local synaptic signals. However, estimates of the resistance between the spine head and the parent dendrite suggest that compartmentalization is not tight enough to electrically decouple the synapse. Here we show in acute hippocampal slices that spine compartmentalization is initially very weak, but increases dramatically upon postsynaptic depolarization. Using NMDA receptors as voltage sensors, we provide evidence that spine necks not only regulate diffusional coupling between spines and dendrites, but also control local depolarization of the spine head. In spines with high-resistance necks, presynaptic activity alone was sufficient to trigger calcium influx through NMDA receptors and R-type calcium channels. We conclude that calcium influx into spines, a key trigger for synaptic plasticity, is dynamically regulated by spine neck plasticity through a process of electrical compartmentalization.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
1529-2401
pubmed:author
pubmed:issnType
Electronic
pubmed:day
10
pubmed:volume
28
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
13457-66
pubmed:meshHeading
pubmed:year
2008
pubmed:articleTitle
Spine neck plasticity controls postsynaptic calcium signals through electrical compartmentalization.
pubmed:affiliation
Friedrich Miescher Institute, Maulbeerstrasse 66, CH-4058 Basel, Switzerland.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't