Cortical gamma band synchronization through somatostatin interneurons

Abstract

Gamma band rhythms may synchronize distributed cell assemblies to facilitate information transfer within and across brain areas, yet their underlying mechanisms remain hotly debated. Most circuit models pose that soma-targeting parvalbumin (PV) positive GABAergic neurons are the essential inhibitory neuron subtype necessary for gamma rhythms. Using cell-type specific optogenetic manipulations in behaving animals, we show that dendrite-targeting somatostatin (SOM) interneurons are critical for a visually induced, context-dependent gamma rhythm in the visual cortex (V1). A novel computational model independently predicts that context-dependent gamma rhythms depend critically on SOM interneurons. Further in vivo experiments show that SOM neurons are required for long distance coherence across V1. Taken together, these data establish a new mechanism for synchronizing distributed networks in the visual cortex. By operating through dendritic and not just somatic inhibition, SOM-mediated oscillations may expand the computational power of gamma rhythms for optimizing the synthesis and storage of visual perceptions.

Synaptic Mechanisms of Feature Coding in the Visual Cortex of Awake Mice

“…Control trials were interleaved with trials in which the cortex was illuminated with an optic fiber coupled to a red LED. Under identical experimental conditions, extracellular recording from SOM cells revealed a 67±8% decrease in SOM firing for the largest stimulus size (Veit et al, 2017). Consistent with the reduced surround suppression observed during their inactivation (~30% decrease for ~57% suppression of SOM firing) (Adesnik et al, 2012), optogenetic suppression of SOM cells substantially increased both visually evoked E and I (E: p < 0.0005, I: p < 0.005, two-way-ANOVA, n = 8, Figure 8B,C), but did not eliminate the size-dependent decrement in the E/I ratio (p > 0.05, two-way-ANOVA, Fig.…”

“…Superficially, the increase in I seems paradoxical, as the direct inhibition from SOM cells should be reduced. However, this paradoxical effect is precisely a core prediction of the ISN regime (Litwin-Kumar et al, 2016; Rubin et al, 2015; Tsodyks et al, 1997); when SOM cells are suppressed, PV cells firing rates substantially increase (Veit et al, 2017). In the ISN model, the increased activity of PV cells is a result of increased drive from L2/3 excitatory neurons (which are net disinhibited).…”

“…The increased activity of PV neurons drives net increases in inhibitory currents in excitatory neurons. A second explanation for the increase in I that does not invoke ISN dynamics is that SOM cells directly inhibit PV neurons (Pfeffer et al, 2013), and thus suppressing SOM cells should result in increased somatic inhibition in pyramidal cells since PV neurons are themselves disinhibited (Veit et al, 2017). The data presented here are similar to what has been recently found for sound frequency tuning in the awake auditory cortex (Kato et al, 2017), implying these might be general mechanisms for feature coding across sensory cortex.…”

Sensory coding is impaired in rat absence epilepsy

“…; Veit et al . ), we hypothesized that GAERS could present a layer‐specific increase of interneurons density, especially of PV+ or SOM+ cells. Recent studies indicated modifications of GABAergic interneurons densities in models of genetic epilepsy that further support our hypothesis (Wimmer et al .…”

“…; Buzsáki & Wang, ; Veit et al . ), an increased number of these interneurons could explain the augmented gamma power in GAERS that not only favours SWDs, but also may alter sensory coding. A recent study showed no difference in terms of GABA+ interneurons in the S1Bf of GAERS (Bombardi et al .…”