Abstract

Visual perception in natural environments depends on the ability to focus on salient stimuli while ignoring distractions. This kind of selective visual attention is associated with gamma activity in the visual cortex. While the nucleus reticularis thalami (nRT) has been implicated in selective attention, its role in modulating gamma activity in the visual cortex remains unknown. Here, we show that somatostatin- (SST) but not parvalbumin-expressing (PV) neurons in the visual sector of the nRT preferentially project to the dorsal lateral geniculate nucleus (dLGN), and modulate visual information transmission and gamma activity in primary visual cortex (V1). These findings pinpoint the SST neurons in nRT as powerful modulators of the visual information encoding accuracy in V1 and represent a novel circuit through which the nRT can influence representation of visual information.

Highlights

  • Visual perception relies on the ability to focus on important information while ignoring distractions

  • We found that the input from nucleus reticularis thalami (nRT) to the dorsal lateral geniculate nucleus (dLGN) in the mouse is predominantly from the class of Neuroscience inhibitory neurons that express SST, with negligible anatomical connections from the more numerous PV-positive neurons (Figure 1, Figure 1—figure supplement 1)

  • Optogenetic activation of SST nRT neurons in alert, head-fixed mice suppressed the SU spiking and field potential responses to visual stimulation in both dLGN and V1, and caused suppression of gamma, whether the mice were stationary or running on a polystyrene ball floating on air

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Summary

Introduction

Visual perception relies on the ability to focus on important information while ignoring distractions. Such selective attention is associated with neural oscillations in the gamma frequency band (~30–90 Hz, ‘gamma oscillations’) in the visual cortices in both rodents and humans (Engel et al, 2001; Taylor et al, 2005; Pavlova et al, 2006; Doesburg et al, 2008; Ray et al, 2008; Siegel et al, 2008). The activity in dLGN is controlled by inputs from GABAergic neurons from the nucleus reticularis thalami (nRT)

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