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This Article Full Text Full Text (PDF) All Versions of this Article: 586/6/1475    most recent jphysiol.2007.148353v1 Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Google Scholar Articles by Bloodgood, B. L. Articles by Sabatini, B. L. PubMed PubMed Citation Articles by Bloodgood, B. L. Articles by Sabatini, B. L. Related Collections Review articles Neuroscience

¹ Department of Neurobiology, Harvard Medical School, 220 Longwood Avenue, Boston, MA 02115, USA

Activation of glutamatergic synapses onto pyramidal neurons produces a synaptic depolarization as well as a buildup of intracellular calcium (Ca²⁺). The synaptic depolarization propagates through the dendritic arbor and can be detected at the soma with a recording electrode. Current influx through AMPA-type glutamate receptors (AMPARs) provides the depolarizing drive, and the amplitudes of synaptic potentials are generally thought to reflect the number and properties of these receptors at each synapse. In contrast, synaptically evoked Ca²⁺ transients are limited to the spine containing the active synapse and result primarily from Ca²⁺ influx through NMDA-type glutamate receptors (NMDARs). Here we review recent studies that reveal that both synaptic depolarizations and spine head Ca²⁺ transients are strongly regulated by the activity of postsynaptic, non-glutamate receptor ion channels. In hippocampal pyramidal neurons, voltage- and Ca²⁺-gated ion channels located in dendritic spines open as downstream consequences of glutamate receptor activation and act within a complex signalling loop that feeds back to regulate synaptic signals. Dynamic regulation of these ion channels offers a powerful mechanism of synaptic plasticity that is independent of direct modulation of glutamate receptors.

(Received 20 November 2007; accepted after revision 14 December 2007; first published online 20 December 2007)
Corresponding author B. Sabatini: Department of Neurobiology, Harvard Medical School, 220 Longwood Avenue, Boston, MA 02115, USA. Email: bsabatini{at}hms.harvard.edu

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