ArticleNeuroscience2013
Terminals of the major thalamic input to visual cortex are devoid of synapsin proteins.
Article in Neuroscience, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 11 citations in OpenAlex.
- Corticosterone-linked microglial activity underpins sexually dimorphic neuroplasticity after ketamine anesthesia.Science advances · 2026Article
- Altered GABAInternational journal of molecular sciences · 2022Article
- VGLUT3 neurons in median raphe control the efficacy of spatial memory retrieval via ETV4 regulation of VGLUT3 transcription.Science China. Life sciences · 2022Article
- Molecular composition of the human primary visual cortex profiled by multimodal mass spectrometry imaging.Brain structure & function · 2018Article
- Ultrastructure of geniculocortical synaptic connections in the tree shrew striate cortex.The Journal of comparative neurology · 2016Article
- Functions of synapsins in corticothalamic facilitation: important roles of synapsin I.The Journal of physiology · 2015Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
Abstract
Synapsins are nerve-terminal proteins that are linked to synaptic transmission and key factors in several forms of synaptic plasticity. While synapsins are generally assumed to be ubiquitous in synaptic terminals, whether they are excluded from certain types of terminals is of interest. In the visual pathway, synapsins are lacking in photoreceptor and bipolar cell terminals as well as in retinogeniculate synapses. These are the terminals of the first three feedforward synapses in the visual pathway, implying that lack of synapsins may be a common property of terminals that provide the primary driver activity onto their postsynaptic neurons. To further investigate this idea, we studied the fourth driver synapse, thalamocortical synapses in visual cortex, using glutamatergic terminal antibody markers anti-VGluT1 and VGluT2, anti-Synapsin I and II, and confocal microscopy to analyze co-localization of these proteins in terminals. We also used pre-embedding immunocytochemical labeling followed by electron microscopy to investigate morphological similarities or differences between terminals containing synapsins or VGluT2. In visual cortex, synapsin coincided extensively with non-TC-neuron marker, VGluT1, while thalamocortical terminal marker VGluT2 and synapsin overlap was sparse. Morphologically, synapsin-stained terminals were smaller than non-stained, while VGluT2-positive thalamocortical terminals constituted the largest terminals in cortex. The size discrepancy between synapsin- and VGluT2-positive terminals, together with the complementary staining patterns, indicates that thalamocortical synapses are devoid of synapsins, and support the hypothesis that afferent sensory information is consistently transmitted without the involvement of synapsins. Furthermore, VGluT2 and synapsins were colocalized in other brain structures, suggesting that lack of synapsins is not a property of VGluT2-containing terminals, but a property of primary driver terminals in the visual system.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.