The lateral geniculate nucleus (LGN) relays visual information from the retina to the primary visual cortex (V1). In addition to glutamatergic fibers from the retina, the neurons in the LGN are innervated by glutamatergic fibers descending from V1. Although corticothalamic feedback fibers outnumber fibers ascending from the retina 10:1, the excitatory drive they provide is quite limited due to the dendritic location and low transmitter release probability of the synapses. While feedback is below the threshold for initiating action potentials, it could modulate the transfer of information to V1. This modulation could provide a mechanism for attention to emphasize behaviorally relevant sensory input. To investigate a role in attention we first identified that the vesicular glutamate transporter type 1 (VGLUT1) is important for the normal function of the feedback neurons and then proceeded to test mice with deficient VGLUT1 expression in a behavioral task that assesses visual attention. EPSCs of corticothalamic origin, measured in wholecell patch-clamp in LGN slices, were absent in VGLUT1 knock-out mice. In heterozygous VGLUT1 mice, corticothalamic synapses had altered short-term plasticity. When VGLUT1-heterozygous mice were subjected to the 5-Choise Serial Reaction Time Task, they had reduced performance in spatially divided attention and inhibitory response control. This could be an effect from an altered corticothalamic modulation of the thalamic relay.
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