The Visual Pathway for Binocular Integration
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RESEARCH HIGHLIGHT
The Visual Pathway for Binocular Integration Na Li1 • Yu Gu1
Received: 14 January 2020 / Accepted: 13 February 2020 Ó Shanghai Institutes for Biological Sciences, CAS 2020
It is generally believed that the visual pathways from each eye do not integrate to form binocular vision until they reach the primary visual cortex (V1), and individual neurons in the visual thalamus (dorsal lateral geniculate nucleus, dLGN) are thought to receive retinal inputs from either the contralateral or the ipsilateral eye [1]. But recently, many lines of anatomical and functional evidence in mice and marmosets have reported that dLGN neurons have binocular responses and binocularly-modulated responses [2]. It is also generally accepted that monocular deprivation (MD) leads to a series of anatomical and functional changes in V1 during the critical period of development, so the question is whether these changes also occur in the dLGN. Recent studies have reported that MD leads to anatomical changes in thalamocortical projections and impairments of specific dLGN cell types and synapses [3]. A rapid ocular dominance shift in the mouse dLGN has been demonstrated after short-term (6–8 days) MD in both young and adult mice, similar to that reported in V1 long ago [4]. However, using long-term MD, researchers failed to detect changes in the visual responses of dLGN neurons similar to those of V1 [5]. Recently, a report by Huh et al. published in the Journal of Neuroscience addressed this question [6]. They focused on two points: whether dLGN neuronal properties are chronically altered after long-term MD during the critical period, and whether the long-lasting deficits attributed to MD during the critical period, in V1 originate in the thalamus.
& Yu Gu [email protected] 1
State Key Laboratory of Medical Neurobiology and Ministry of Education Frontiers Center for Brain Science, Institutes of Brain Science, Fudan University, Shanghai 200032, China
To determine which functional properties of dLGN neurons are changed after long-term MD, the authors injected Cre-dependent GCaMP6s virus (AAV1.Syn.Flex.GCaMP6s virus) into the dLGN of VGLUT2-Cre mice (Vglut2-irescre) which restricted GCaMP6s expression specifically to dLGN neurons. After MD for 14 days during the critical period, they tested the changes in visual functions of dLGN boutons projecting to V1 through in vivo two-photon calcium imaging. Interestingly, in addition to ocular dominance plasticity, the number and fraction of binocular dLGN boutons were significantly reduced. In other words, the binocular thalamocortical inputs underwent a profound loss after long-term MD. While MD had no evident impact on the overall preferred spatial frequency of dLGN boutons, other visual properties of these boutons, such as binocular matching and binocular modulation, were also evidently changed. Following long-term MD during the critical period, binocular thalamocortical inputs were mismatched in multiple visual response properties, such as t
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