ArticleMolecular neurobiology2026
Intranasal 6-OHDA Induces TRPM3-mediated Neuroinflammation in the pVTA: A Preclinical Early-stage Parkinson's Disease Model.
Article in Molecular neurobiology, 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
5 authors.
Funding
Abstract
Parkinson's disease (PD) is a progressive neurodegenerative disorder marked by motor impairment, but early-stages are dominated by non-motor symptoms such as olfactory dysfunction, anxiety, depression, and cognitive deficits, which are poorly replicated by currently studied animal models. In animal models of PD, stereotaxic injection of 6-hydroxydopamine (6-OHDA) into the substantia nigra induces dopaminergic neurodegeneration, which consequently produces motor deficits; but inadequately representing early non-motor features. Emerging evidence suggests that transient receptor potential melastatin 3 (TRPM3)-associated neuroinflammation may contribute to early PD progression and non-motor symptoms. However, its role in early-stage PD, particularly in non-invasive models, remains unclear. Therefore, this study aimed to develop a novel non-invasive early-stage PD model and investigate TRPM3-associated neuroinflammation. Early-stage PD-like symptoms were induced in rats by intranasal 6-OHDA (5 mg/nostril) for 7 consecutive days and evaluated using the buried food, odor identification, open field, and elevated plus maze tests. Tyrosine hydroxylase (TH) immunoreactivity was quantified in the olfactory bulb, ventral striatum, and posterior ventral tegmental area (pVTA). TRPM3 immunoreactivity, neuroplastic changes in the pVTA and interleukin-1β (IL-1β) in the ventral striatum and pVTA were also assessed. 6-OHDA produced behavioral deficits, reduced TH immunoreactivity, increased TRPM3, elevated IL-1β, and impaired pVTA neuroplasticity. Intraperitoneal (i.p.) treatment of TRPM3 inhibitor primidone (2.5, 5, and 10 mg/kg) significantly reversed these alterations, and standard pramipexole (3 mg/kg, i.p.) also reduced behavioral deficits. Overall, the intranasal 6-OHDA model reproduces key features of early-stage PD, including non-motor deficits, dopaminergic dysfunction, TRPM3-associated neuroinflammation, and impaired neuroplasticity, providing a simple and clinically relevant platform for therapeutic evaluation.
Indexed as
Identifiers
42470577What 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.