QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

HOME  |   SEARCH  |   ARCHIVE  |   SUBSCRIBE  |   CONTACT  |   HELP

The Journal of Neuroscience, July 15, 2009, 29(28):9127-9136; doi:10.1523/JNEUROSCI.5971-08.2009

This Article Full Text Full Text (PDF) Supplemental Data Submit an eLetter Alert me when this article is cited Alert me when eLetters are posted Alert me if a correction is posted Citation Map 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 Google Scholar Google Scholar Articles by Hull, C. Articles by Scanziani, M. Search for Related Content PubMed PubMed Citation Articles by Hull, C. Articles by Scanziani, M.

 Previous Article

Cellular/Molecular
Postsynaptic Mechanisms Govern the Differential Excitation of Cortical Neurons by Thalamic Inputs

Court Hull,¹ Jeffry S. Isaacson,² and Massimo Scanziani¹

¹Neurobiology Section, Division of Biology, and ²Neuroscience Department, School of Medicine, University of California, San Diego, La Jolla, California 92093-0634

Correspondence should be addressed to Massimo Scanziani, Neurobiology Section 0634, Division of Biology, University of California, San Diego, 9500 Gilman Drive, La Jolla, CA 92093-0634. Email: massimo{at}biomail.ucsd.edu

Thalamocortical (TC) afferents relay sensory input to the cortex by making synapses onto both excitatory regular-spiking principal cells (RS cells) and inhibitory fast-spiking interneurons (FS cells). This divergence plays a crucial role in coordinating excitation with inhibition during the earliest steps of somatosensory processing in the cortex. Although the same TC afferents contact both FS and RS cells, FS cells receive larger and faster excitatory inputs from individual TC afferents. Here, we show that this larger thalamic excitation of FS cells occurs via GluR2-lacking AMPA receptors (AMPARs), and results from a fourfold larger quantal amplitude compared with the thalamic inputs onto RS cells. Thalamic afferents also activate NMDA receptors (NMDARs) at synapses onto both cells types, yet RS cell NMDAR currents are slower and pass more current at physiological membrane potentials. Because of these synaptic specializations, GluR2-lacking AMPARs selectively maintain feedforward inhibition of RS cells, whereas NMDARs contribute to the spiking of RS cells and hence to cortical recurrent excitation. Thus, thalamic afferent activity diverges into two routes that rely on unique complements of postsynaptic AMPARs and NMDARs to orchestrate the dynamic balance of excitation and inhibition as sensory input enters the cortex.

---

Received Dec. 15, 2008; revised May 31, 2009; accepted June 17, 2009.

Correspondence should be addressed to Massimo Scanziani, Neurobiology Section 0634, Division of Biology, University of California, San Diego, 9500 Gilman Drive, La Jolla, CA 92093-0634. Email: massimo{at}biomail.ucsd.edu

Home  |   Search  |   Archive  |   Subscribe  |   Contact  |   Help