The parabigeminal nucleus is a source of “retinogeniculate replacement terminals” in mice that lack retinofugal input

Abstract

In the dorsal lateral geniculate nucleus (LGN) of mice that lack retinal input, a population of large terminals supplants the synaptic arrangements normally made by the missing retinogeniculate terminals. To identify potential sources of these "retinogeniculate replacement terminals," we used mutant mice (math5 -/-) which lack retinofugal projections due to the failure of retinal ganglion cells to develop. In this line, we labeledLGN terminals that originate from the primary visual cortex (V1) or the parabigeminal nucleus (PBG), and compared their ultrastructure to retinogeniculate, V1 or PBG terminals in the dLGN of C57Blk6 (WT) mice (schematically depicted above graph).Corticogeniculate terminals labeled in WT and math5 -/mice were similar in size and both groups were significantly smaller than WT retinogeniculate terminals. In contrast, the PBG projection in math5 -/mice was extensive and there was considerable overlap in the sizes of retinogeniculate terminals in WT mice and PBG terminals in math5 -/mice (summarized in histogram). The data indicate that V1 is not a source of "retinogeniculate replacement terminals" and suggests that large PBG terminals expand their innervation territory to replace retinogeniculate terminals in their absence.

Cell-type specific binocular interactions in mouse visual thalamus

“…While these interactions could be mediated by extrinsic sources (e.g. cortex, 39 ; thalamic reticular nucleus, 40,41 ; superior colliculus, 42 ; pretectum, 43,44 ; or parabigeminal nucleus, 29,45 ), our study indicates that geniculate interneurons provide one of the first locations where signals from the two eyes can be compared, integrated, and adjusted before being transmitted to cortex. Whether these interneuron-mediated binocular interactions translate to species where retinogeniculate inputs from the two eyes are more highly segregated and arranged in a laminar fashion, requires additional investigation.…”

“…The physiological responses recorded in our study corroborate the known anatomical connections within the dLGN. Whyland et al, 29 found no significant differences in the sizes of contralateral and ipsilateral retinogeniculate terminals in the mouse and no difference in the proportion of their synaptic contacts on interneurons (ipsilateral 12%, contralateral 13%) and relay cells (ipsilateral 88%, contralateral 87%). Thus, although ipsilateral and contralateral retinogeniculate terminals originate from different subsets of retinal ganglion cells 30 , they do not differentially innervate relay cells versus interneurons.…”

Loss of Retinogeniculate Synaptic Function in the DBA/2J Mouse Model of Glaucoma

“…This result is consistent with findings from the superior colliculus, where anterograde transport loss precedes synaptic loss ( Crish et al, 2010 ; Smith et al, 2016 ). However, some remaining vGlut2 signal might also originate from tectogeniculate synaptic inputs arising from vGlut2-expressing projection neurons in the stratum griseum superficiale of the superior colliculus ( Fremeau et al, 2001 ; Bickford et al, 2015 ) or potentially other “replacement terminals” ( Whyland et al, 2022 ).…”

Development of feedforward and feedback connections between the dorsal lateral geniculate nucleus and the thalamic reticular nucleus

“…This mutant lacks the transcription factor Math5, which is essential for the differentiation of retinal progenitors into retinal ganglion cells. As a result, Math5 −/− mice exhibit a wholesale loss (> 95%) of retinal ganglion cells, a failure to develop an optic nerve, and a brain that is devoid of retinofugal projections [31][32][33][34]. Finally, because our focus is on visual intrathalamic circuits, we also assessed whether the modality-speci c sectors of TRN were present at birth and if such an arrangement was altered by visual deafferentation.…”