Abstract
Neuronal oscillations are a ubiquitous feature of thalamocortical networks and can be dynamically modulated across processing states, enabling thalamocortical communication to flexibly adapt to varying environmental and behavioral demands. The lateral geniculate nucleus (LGN), like all thalamic nuclei, engages in reciprocal synaptic interactions with the cortex, relaying retinal information to and receiving feedback input from primary visual cortex (V1). While retinal excitation is the primary driver of LGN activity, retinal synapses represent a minority of the total synaptic input onto LGN neurons, allowing for both retinogeniculate and geniculocortical signals to be influenced by nonretinal sources. To gain a holistic view of network processing in the geniculocortical pathway, we performed simultaneous extracellular recordings from the LGN and V1 of behaving macaque monkeys, measuring local field potentials (LFPs) and spiking activity. These recordings revealed prominent beta-band oscillations coherent between the LGN and V1 that influenced spike timing in the LGN and were statistically consistent with a feedforward process from the LGN to V1. These thalamocortical oscillations were suppressed by visual stimulation, spatial attention, and behavioral arousal, strongly suggesting that these oscillations are not a feature of active visual processing. Instead, they appear analogous to occipital lobe, alpha oscillations recorded in humans and may represent a signature of signal suppression that occurs during periods of low engagement or active distractor suppression.
Significance Statement
Oscillations within thalamocortical networks in the awake state are generally believed to enhance communication between the thalamus and cortex, allowing circuits to flexibly respond to changes in sensory, behavioral, and cognitive demands. Here, we show that oscillations within and between the LGN and V1 are suppressed by increases in visual stimulation, increases in behavioral arousal, and shifts in covert spatial attention. We therefore conclude that these oscillations are not a mechanism to enhance the transmission of retinal information through the LGN to V1. Instead, we propose that they are a signature of signal suppression that occurs when network engagement is low or during active distractor suppression.
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