ArticleNeurochemical research2026
Striatal Dopamine D2 Receptors Contribute to N-Ethylpentylone-Induced Arousal in Mice.
Article in Neurochemical 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
10 authors.
Funding
Abstract
Drug-induced sleep disruption exacerbates addiction, causes long-term cognitive and emotional deficits, and becomes a key relapse trigger. However, despite the potent stimulant and hallucinogenic effects of synthetic cathinones, their impact on sleep-wake behaviors remains unstudied, and the role of striatal dopamine D2 receptors in mediating psychostimulant-induced arousal has yet to be identified. This study aimed to elucidate the mechanisms underlying N-ethylpentylone (NEP, a second-generation synthetic cathinone) induced alterations in sleep-wake behavior, specifically investigating the relative contributions of dopamine receptors (DARs) and serotonin receptors. Using the in vitro PRESTO-Tango assay, we characterized the interactions between NEP and various DARs, revealing that NEP produced the strongest β-arrestin recruitment response at dopamine D2 receptor (D2R) among the dopamine receptor subtypes tested. In vivo electroencephalogram/electromyogram (EEG/EMG) recordings in wild-type (WT) mice demonstrated that NEP dose-dependently promoted wakefulness and reduced non-rapid eye movement (NREM) sleep. This was accompanied by decreased θ-band and increased α-band power spectral density during wakefulness. Pharmacological blockade of D2R with haloperidol significantly attenuated NEP-induced wake promotion and partially reversed the aberrant EEG oscillations. Crucially, conditional knockout of D2R specifically in striatum markedly diminished the wake-promoting effects of NEP. In contrast, pharmacological blockade of the serotonin 2 A receptor (5-HT2AR) with 1 mg/kg MDL100907 did not significantly alter NEP-induced sleep-wake changes. Furthermore, immunofluorescence staining analysis confirmed that D2R blockade effectively reversed NEP-induced c-Fos expression in the striatum. Together, these findings demonstrated striatal D2R played a critical role in NEP-induced arousal.
Indexed as
Identifiers
42545657What Socratic 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 Socratic graph.