ArticleNeural regeneration research2026
Thalamic reticular nucleus in the pathophysiology of schizophrenia.
Article in Neural regeneration research, 2026. 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
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mechanistic analyses on schizophrenia have traditionally focused on corticolimbic structures such as the prefrontal cortex, hippocampus, and amygdala, given their established roles in cognition. However, the thalamus, a critical hub that interconnects these regions, has garnered comparatively less attention. Of particular interest is the thalamic reticular nucleus, which plays a crucial role in cognition and sensory processing through its connections with the dorsomedial thalamic nucleus and the prefrontal cortex. A potential role of the thalamic reticular nucleus in schizophrenia has been suggested in a few reports; however, recent analyses have identified a specific link between the thalamic reticular nucleus and layer 5 neurons of the prefrontal cortex, a relationship highlighted by our group's earlier findings from 2012, which demonstrated that bilateral thalamic reticular nucleus lesions in adult rats caused neuronal atrophy in these cortical neurons. Building on this foundation, this manuscript explores the role of the thalamic reticular nucleus in schizophrenia neurobiology by reviewing its functional neuroanatomy, its integration within the corticolimbic system, and mechanisms of its potential involvement in the disease. This hypothesis is further developed by describing our novel findings from rats with neonatal ventral hippocampus lesion, widely considered a developmental model for schizophrenia. For the first time, we report dendritic spine pathology in thalamic reticular nucleus neurons, characterized by reduced spine density and a lower proportion of mushroom spines. Furthermore, we demonstrate a decrease in the density of parvalbumin-positive cells within the thalamic reticular nucleus in the neonatal ventral hippocampus lesion model. Together, these findings suggest significant alterations in the corticolimbic network and position the thalamic reticular nucleus as a complex yet promising mechanistic contributor to the neurobiology of schizophrenia.
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.