4.6 Article

Amplifying the redistribution of somato-dendritic inhibition by the interplay of three interneuron types

Journal

PLOS COMPUTATIONAL BIOLOGY
Volume 15, Issue 5, Pages -

Publisher

PUBLIC LIBRARY SCIENCE
DOI: 10.1371/journal.pcbi.1006999

Keywords

-

Funding

  1. German Federal Ministry for Education and Research [FKZ 01GQ1201]

Ask authors/readers for more resources

GABAergic interneurons play an important role in shaping the activity of excitatory pyramidal cells (PCs). How the various inhibitory cell types contribute to neuronal information processing, however, is not resolved. Here, we propose a functional role for a widespread network motif consisting of parvalbumin- (PV), somatostatin- (SOM) and vasoactive intestinal peptide (VIP)-expressing interneurons. Following the idea that PV and SOM interneurons control the distribution of somatic and dendritic inhibition onto PCs, we suggest that mutual inhibition between VIP and SOM cells translates weak inputs to VIP interneurons into large changes of somato-dendritic inhibition of PCs. Using a computational model, we show that the neuronal and synaptic properties of the circuit support this hypothesis. Moreover, we demonstrate that the SOM-VIP motif allows transient inputs to persistently switch the circuit between two processing modes, in which top-down inputs onto apical dendrites of PCs are either integrated or cancelled. Author summary Neurons in the brain can be classified as excitatory or inhibitory based on whether they activate or deactivate the cells to whom they send signals. Compared to their excitatory counterpart, inhibitory neurons present themselves as a wild diversity of cell classes. It is broadly believed that these classes serve different purposes, but as of now, those are poorly understood. In this article, we suggest how an intricate interplay of three inhibitory cell classes can control whether internal signalssuch as predictions, memory signals or motor commandsare taken into account when sensory signals are interpreted. Using a mathematical model and computer simulations, we show that such internal signals can be shut down by regulating which inhibitory cell types are active, and that the interaction of different cell classes allows weak control signals to do so.

Authors

I am an author on this paper
Click your name to claim this paper and add it to your profile.

Reviews

Primary Rating

4.6
Not enough ratings

Secondary Ratings

Novelty
-
Significance
-
Scientific rigor
-
Rate this paper

Recommended

No Data Available
No Data Available