DARK EXPOSURE RESHAPES SYNAPTIC AND NETWORK INFORMATION PROCESSING IN THE DORSAL LATERAL GENICULATE NUCLEUS

The dorsal lateral geniculate nucleus (dLGN) is a central hub in the visual pathway that has recently emerged as a site of experience-dependent plasticity, actively processing visual information rather than simply relaying retinal inputs to higher visual areas. Visual deprivation provides a powerful paradigm to study adaptive plasticity in the visual system. Several studies showed indeed that visual deprivation reshapes cortical plasticity in the adult mouse brain. However, its impact on information processing in the dLGN in vivo remains unclear.
Here, we investigate how dark exposure (DE) alters synaptic and network function in the adult mouse visual thalamus. Using ex-vivo patch-clamp recordings and fluorescent in situ hybridization, we observed that 7 days of dark exposure induces homeostatic synaptic plasticity in the dLGN, characterized by enhanced short-term depression of retinogeniculate transmission. This effect may arise from increased presynaptic release probability together with an upregulation of the AMPA receptor auxiliary subunit CKAMP44, which slows recovery from receptor desensitization, as supported by data from CKAMP44^-/- mice recordings.
To assess the impact of these homeostatic changes on visual information processing in the thalamus, we perform in vivo Neuropixels chronic recordings from dLGN in head-fixed awake mice while presenting visual stimuli. By analysing firing rates dynamics, response reliability, and tuning before and after 7 days of DE, we investigate how DE reshapes thalamic computation. Based on our data and previous studies, we hypothesize that homeostatic plasticity at retinogeniculate synapses alters the population code in the dLGN by dynamically adjusting gain, temporal filtering, and tuning properties.