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This Article Full Text Full Text (PDF) Supplemental Data All Versions of this Article: 585/2/447    most recent jphysiol.2007.142315v1 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 Citing Articles via Google Scholar Google Scholar Articles by Milojkovic, B. A. Articles by Antic, S. D. Search for Related Content PubMed PubMed Citation Articles by Milojkovic, B. A. Articles by Antic, S. D. Related Collections Neuroscience Related Article

¹ Department of Neurobiology, Yale University School of Medicine, 333 Cedar Street, New Haven, CT 06510, USA
² Department of Neuroscience, UConn Health Center, 263 Farmington Avenue, Farmington, CT 06030, USA

Higher cortical functions (perception, cognition, learning and memory) are in large part based on the integration of electrical and calcium signals that takes place in thin dendritic branches of neocortical pyramidal cells (synaptic integration). The mechanisms underlying the synaptic integration in thin basal dendrites are largely unexplored. We use a recently developed technique, multisite voltage–calcium imaging, to compare voltage and calcium transients from multiple locations along individual dendritic branches. Our results reveal characteristic electrical transients (plateau potentials) that trigger and shape dendritic calcium dynamics and calcium distribution during suprathreshold glutamatergic synaptic input. We regularly observed three classes of voltage–calcium interactions occurring simultaneously in three different zones of the same dendritic branch: (1) proximal to the input site, (2) at the input site, and (3) distal to the input site. One hundred micrometers away from the synaptic input site, both proximally and distally, dendritic calcium transients are in tight temporal correlation with the dendritic plateau potential. However, on the same dendrite, at the location of excitatory input, calcium transients outlast local dendritic plateau potentials by severalfold. These Ca²⁺ plateaus (duration 0.5–2 s) are spatially restricted to the synaptic input site, where they cause a brief down-regulation of dendritic excitability. Ca²⁺ plateaus are not mediated by Ca²⁺ release from intracellular stores, but rather by an NMDA-dependent small-amplitude depolarization, which persists after the collapse of the dendritic plateau potential. These unique features of dendritic voltage and calcium distributions may provide distinct zones for simultaneous long-term (bidirectional) modulation of synaptic contacts along the same basal branch.

(Received 1 August 2007; accepted after revision 4 October 2007; first published online 11 October 2007)
Corresponding author S. D. Antic: Department Neuroscience, L-4000, UConn Health Center, 263 Farmington Ave., Farmington, CT 06030-3401, USA. Email: antic{at}neuron.uchc.edu

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