Effects of GABAa somatic inhibition on orientation tuning and contrast sensitivity in visual cortex

Abstract

Event Abstract Back to Event Effects of GABAa somatic inhibition on orientation tuning and contrast sensitivity in visual cortex The selectivity of neurons in sensory cortex is thought to be at least partially shaped by inhibitory connections. In primary visual cortex (V1) many studies have examined how orientation tuning is affected by application of the GABAa antagonist bicuculline. These studies, however, have reported inconsistent results: some have seen a loss of selectivity and others only minor effects. A possible reason lies in the broad spectrum of effects of bicuculline; much more selective blockage of GABAa receptors is achieved with the potent antagonist gabazine (SR95531). We examined the effect of local gabazine iontophoresis on orientation tuning in V1 of anesthetized cats. Using extracellular recordings, we measured orientation tuning with drifting gratings. Gabazine was iontophoresed immediately above the recording electrode. An array of 96 electrodes was placed ~0.5 mm away to examine the spatial spread of gabazine. If gabazine did not affect responses measured with the array, we assumed that its effects were mostly restricted to the soma and proximal dendrites of neurons at the site of iontophoresis. Blocking GABAa-receptor mediated, somatic inhibition increased responses to all orientations by 150%, broadened tuning width by 22%, and reduced direction selectivity by 32% (medians, n=23). The resulting tuning curves resembled responses typically measured in subthreshold membrane potential, suggesting that GABAa provides untuned inhibition, keeping responses to most orientations below threshold. We tested this hypothesis using a simple rectification model. The model relies on the finding that the shape of orientation tuning curves for firing rates can be predicted by applying an appropriate threshold and gain to noisy membrane potential responses. Given these parameters, we sought to determine two hypothetical membrane potential tuning curves, which were allowed to differ only in their mean responses across orientations, to predict the tuning curve for firing rates in both the control and gabazine condition. This rectification model captured the observed effects of blocking GABAa-receptor mediated, somatic inhibition, i.e. increase in responses, broadening of orientation tuning, and decrease of direction selectivity. The success of the model suggests that inhibition hyperpolarizes the membrane potential by a constant amount, resulting in fewer threshold crossings, and therefore decreased firing rates and increased selectivity. Next, we asked whether inhibition depended on overall contrast. We measured contrast response functions with drifting gratings of optimal orientation before, during, and after gabazine administration. Blocking inhibition led to increases in firing rates that were stronger for high-contrast than for low-contrast stimuli. These effects are consistent with the notion that inhibition grows with contrast. We conclude that GABAa-receptor mediated, somatic inhibition plays an important role in orientation and direction selectivity by keeping membrane potential responses to most stimulus orientations below threshold, but not necessarily by shaping the tuning curve itself. Our results are consistent with the view that somatic inhibition provides a constant hyperpolarization, whose magnitude depends on stimulus contrast, but not on orientation. Support: NIH EY017396. Conference: Computational and systems neuroscience 2009, Salt Lake City, UT, United States, 26 Feb - 3 Mar, 2009. Presentation Type: Poster Presentation Topic: Poster Presentations Citation: (2009). Effects of GABAa somatic inhibition on orientation tuning and contrast sensitivity in visual cortex. Front. Syst. Neurosci. Conference Abstract: Computational and systems neuroscience 2009. doi: 10.3389/conf.neuro.06.2009.03.203 Copyright: The abstracts in this collection have not been subject to any Frontiers peer review or checks, and are not endorsed by Frontiers. They are made available through the Frontiers publishing platform as a service to conference organizers and presenters. The copyright in the individual abstracts is owned by the author of each abstract or his/her employer unless otherwise stated. Each abstract, as well as the collection of abstracts, are published under a Creative Commons CC-BY 4.0 (attribution) licence (https://creativecommons.org/licenses/by/4.0/) and may thus be reproduced, translated, adapted and be the subject of derivative works provided the authors and Frontiers are attributed. For Frontiers’ terms and conditions please see https://www.frontiersin.org/legal/terms-and-conditions. Received: 03 Feb 2009; Published Online: 03 Feb 2009. 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