HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) Supplemental Material All Versions of this Article: 101/1/207    most recent 01280.2007v1 Alert me when this article is cited 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 Karameh, F. N. Articles by Massaquoi, S. G. Search for Related Content PubMed PubMed Citation Articles by Karameh, F. N. Articles by Massaquoi, S. G.

Intracortical Augmenting Responses in Networks of Reduced Compartmental Models of Tufted Layer 5 Cells

¹Department of Electrical and Computer Engineering, American University of Beirut, Beirut, Lebanon; and ²Department of Electrical Engineering and Computer Science and ³Massachusetts Institute of Technology–Harvard Division of Health Sciences and Technology, Massachusetts Institute of Technology, Cambridge, Massachusetts

Submitted 15 September 2008; accepted in final form 11 October 2008

Augmenting responses (ARs) are characteristic recruitment phenomena that can be generated in target neural populations by repetitive intracortical or thalamic stimulation and that may facilitate activity transmission from thalamic nuclei to the cortex or between cortical areas. Experimental evidence suggests a role for cortical layer 5 in initiating at least one form of augmentation. We present a three-compartment model of tufted layer 5 (TL5) cells that faithfully reproduces a wide range of dynamics in these neurons that previously has been achieved only partially and in much more complex models. Using this model, the simplest network exhibiting AR was a single pair of TL5 and inhibitory (IN5) neurons. Intracellularly, AR initiation was controlled by low-threshold Ca²⁺ current (I_T), which promoted TL5 rebound firing, whereas AR strength was dictated by inward-rectifying current (I_h), which regulated TL5 multiple-spike firing and also prevented excessive firing under high-amplitude stimuli. Synaptically, AR was significantly more salient under concurrent stimulus delivery to superficial and deep dendritic zones of TL5 cells than under conventional single-zone stimuli. Moreover, slow GABA-B–mediated inhibition in TL5 cells controlled AR strength and frequency range. Finally, a network model of two cortical populations interacting across functional hierarchy showed that intracortical AR occurred prominently upon exciting superficial cortical layers either directly or via intrinsic connections, with AR frequency dictated by connection strength and background activity. Overall, the investigation supports a central role for a TL5–IN5 skeleton network in low-frequency cortical dynamics in vivo, particularly across functional hierarchies, and presents neuronal models that facilitate accurate large-scale simulations.