ArticleVeterinary medicine and science2026
Molecular and Immunohistochemical Analyses of PLIN4 in the Spinal Cord and Brain During the Development of Electroacupuncture-Induced Analgesic Tolerance in Mice.
Article in Veterinary medicine and science, 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
14 authors.
Funding
Abstract
backgroundElectroacupuncture (EA) is an important non-pharmacological approach for pain management in veterinary and human medicine. However, electroacupuncture-induced analgesic tolerance (EAT) limits its long-term efficacy, and the underlying mechanisms remain unclear. Perilipin 4 (Plin4) is a lipid droplet-associated protein involved in lipid storage, lipid droplet dynamics, and cellular lipid homeostasis. Emerging evidence suggests that it also plays a role in neuronal lipid metabolic changes and pain modulation.
objectivesTo investigate the role of Plin4 in the development of EAT and explore its potential as a molecular target for attenuating this limitation.
methodsEAT was induced in male mice by daily 100 Hz EA stimulation for 7 consecutive days. Plin4 expression levels in the amygdala, periaqueductal grey, and spinal cord were examined, and immunofluorescence was used to determine cellular localization. The functional role of Plin4 was assessed by intrathecal Plin4 knockdown in mice and by Plin4 overexpression or knockdown in N2a cells. A total of 99 male mice were used in the primary experiments, with an additional 24 mice used for siRNA knockdown validation in the Supporting Information.
resultsRepeated EA induced analgesic tolerance and markedly upregulated Plin4 in the spinal cord, amygdala, and periaqueductal grey. In the spinal cord, increased Plin4 was mainly localized to spinal cord dorsal horn neurons. Intrathecal Plin4 knockdown delayed EAT onset and increased the pain threshold. In N2a cells, Plin4 expression was positively associated with lipid droplet formation.
conclusionsSpinal neuronal Plin4 contributes to the development of EA-induced analgesic tolerance, possibly by altering neuronal lipid homeostasis. Plin4 may represent a potential molecular target for attenuating tolerance, prolonging EA-induced analgesia, and optimizing EA-based pain management strategies in veterinary medicine.
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.