English
 
User Manual Privacy Policy Disclaimer Contact us
  Advanced SearchBrowse

Item

ITEM ACTIONSEXPORT

Released

Journal Article

Robustness of sensory-evoked excitation is increased by inhibitory inputs to distal apical tuft dendrites

MPS-Authors
/persons/resource/persons84931

Egger,  R
Max Planck Institute for Biological Cybernetics, Max Planck Society;

/persons/resource/persons192641

Schmitt,  AC
Research Group Neural Population Imaging, Max Planck Institute for Biological Cybernetics, Max Planck Society;

/persons/resource/persons84296

Wallace,  DJ
Research Group Neural Population Imaging, Max Planck Institute for Biological Cybernetics, Max Planck Society;

/persons/resource/persons84910

Oberlaender,  M
Max Planck Institute for Biological Cybernetics, Max Planck Society;

/persons/resource/persons84010

Kerr,  JND
Research Group Neural Population Imaging, Max Planck Institute for Biological Cybernetics, Max Planck Society;

External Ressource
Fulltext (public)
There are no public fulltexts stored in PuRe
Supplementary Material (public)
There is no public supplementary material available
Citation

Egger, R., Schmitt, A., Wallace, D., Sakmann, B., Oberlaender, M., & Kerr, J. (2015). Robustness of sensory-evoked excitation is increased by inhibitory inputs to distal apical tuft dendrites. Proceedings of the National Academy of Sciences of the United States of America, 112(45), 14072-14077. doi:10.1073/pnas.1518773112.


Cite as: http://hdl.handle.net/11858/00-001M-0000-002A-43B9-5
Abstract
Cortical inhibitory interneurons (INs) are subdivided into a variety of morphologically and functionally specialized cell types. How the respective specific properties translate into mechanisms that regulate sensory-evoked responses of pyramidal neurons (PNs) remains unknown. Here, we investigated how INs located in cortical layer 1 (L1) of rat barrel cortex affect whisker-evoked responses of L2 PNs. To do so we combined in vivo electrophysiology and morphological reconstructions with computational modeling. We show that whisker-evoked membrane depolarization in L2 PNs arises from highly specialized spatiotemporal synaptic input patterns. Temporally L1 INs and L2–5 PNs provide near synchronous synaptic input. Spatially synaptic contacts from L1 INs target distal apical tuft dendrites, whereas PNs primarily innervate basal and proximal apical dendrites. Simulations of such constrained synaptic input patterns predicted that inactivation of L1 INs increases trial-to-trial variability of whisker-evoked responses in L2 PNs. The in silico predictions were confirmed in vivo by L1-specific pharmacological manipulations. We present a mechanism—consistent with the theory of distal dendritic shunting—that can regulate the robustness of sensory-evoked responses in PNs without affecting response amplitude or latency.