Contrast dependence and differential contributions from somatostatin- and parvalbumin-expressing neurons to spatial integration in mouse V1.

Journal Article (Journal Article)

A characteristic feature in the primary visual cortex is that visual responses are suppressed as a stimulus extends beyond the classical receptive field. Here, we examined the role of inhibitory neurons expressing somatostatin (SOM⁺) or parvalbumin (PV⁺) on surround suppression and preferred receptive field size. We recorded multichannel extracellular activity in V1 of transgenic mice expressing channelrhodopsin in SOM⁺ neurons or PV⁺ neurons. Preferred size and surround suppression were measured using drifting square-wave gratings of varying radii and at two contrasts. Consistent with findings in primates, we found that the preferred size was larger for lower contrasts across all cortical depths, whereas the suppression index (SI) showed a trend to decrease with contrast. We then examined the effect of these metrics on units that were suppressed by photoactivation of either SOM⁺ or PV⁺ neurons. When activating SOM⁺ neurons, we found a significant increase in SI at cortical depths >400 μm, whereas activating PV⁺ neurons caused a trend toward lower SIs regardless of cortical depth. Conversely, activating PV⁺ neurons significantly increased preferred size across all cortical depths, similar to lowering contrast, whereas activating SOM⁺ neurons had no systematic effect on preferred size across all depths. These data suggest that SOM⁺ and PV⁺ neurons contribute differently to spatial integration. Our findings are compatible with the notion that SOM⁺ neurons mediate surround suppression, particularly in deeper cortex, whereas PV⁺ activation decreases the drive of the input to cortex and therefore resembles the effects on spatial integration of lowering contrast.

Full Text

Duke Authors

Cited Authors

  • Nienborg, H; Hasenstaub, A; Nauhaus, I; Taniguchi, H; Huang, ZJ; Callaway, EM

Published Date

  • July 3, 2013

Published In

Volume / Issue

  • 33 / 27

Start / End Page

  • 11145 - 11154

PubMed ID

  • 23825418

Pubmed Central ID

  • PMC3718383

Electronic International Standard Serial Number (EISSN)

  • 1529-2401

Digital Object Identifier (DOI)

  • 10.1523/JNEUROSCI.5320-12.2013

Language

  • eng

Conference Location

  • United States