ArticleJournal of molecular medicine (Berlin, Germany)2025
Neuroanatomical characterization of the cell adhesion molecule IgSF9b reveals localization to inhibitory and excitatory synapses in the mouse limbic system.
Article in Journal of molecular medicine (Berlin, Germany), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
Abstract
Immunoglobulin superfamily member 9b (IgSF9b) is a cell adhesion protein that has been linked to the etiology of several neuropsychiatric disorders, most notably schizophrenia and major depression. Based on previous studies in cultures, IgSF9b was proposed to specifically regulate the structure and function of inhibitory synapses in the brain through an indirect interaction with the synaptic adhesion protein Neuroligin-2 (Nlgn2). However, very little is known about the protein expression pattern of IgSF9b in the intact brain, and the synaptic localization of IgSF9b in different brain regions has never been investigated. To address this question, we conducted an immunohistochemical characterization of IgSF9b expression across the mouse brain and investigated its colocalization with gephyrin, Nlgn2 and VIAAT as markers of GABAergic inhibitory synapses, as well as with PSD-95 and VGLUT1 as markers of glutamatergic excitatory synapses. Unexpectedly, we observed that in the brain regions assessed, only a small fraction of IgSF9b puncta colocalized with inhibitory marker puncta, with a similarly small fraction colocalizing with excitatory synapses. The majority of IgSF9b puncta were not associated with any of the investigated synaptic markers, indicating that IgSF9b may have additional functions beyond those at GABAergic and glutamatergic synapses. Moreover, deletion of IgSF9b resulted in alterations in inhibitory synapse markers in the stratum lacunosum moleculare of hippocampal area CA1 as well as in the lateral and medial habenula, which play key roles in the regulation of cognitive and affective behaviors, respectively. Together, our findings provide an important context for the assessment of the role of IgSF9b in neuropsychiatric disorders. KEY MESSAGES: IgSF9b is expressed in psychiatrically relevant brain regions in the mouse brain. Loss of IgSF9b leads to a small but significant reduction in inhibitory synapses. Only a subset of inhibitory synapses in the regions assessed contain IgSF9b. IgSF9b is additionally present at a subset of excitatory synapses in these regions. Only 20% of IgSF9b is localized to synapses, while the majority is non-synaptic.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.