ArticleNeuropsychopharmacology : official publication of the American College of Neuropsychopharmacology2026
Cannabinoid CB1 receptor and mu-opioid receptor interaction: new insights from conditional knockout mice.
Article in Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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
2 citing papers in PubMed.
- Dissociable control of depression and visceral pain by the pICNeuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2026Article
- Chronic Pain and Opioids in the Elderly: Treating the Brain, Not Just the Body.International journal of environmental research and public health · 2026Review
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
Co-administration of cannabinoids and opioids has been shown to enhance analgesic effects. However, the underlying mechanisms remain unclear. One hypothesis suggests that cannabinoid CB1 receptors (CB1R) and mu-opioid receptors (MOR) interact at the cell membrane or intracellular signaling level. This study aimed to test this hypothesis by examining CB1R-MOR colocalization and assessing whether the deletion of one receptor affects the other's response to its ligand. Results from RNAscope in situ hybridization revealed that CB1R and MOR mRNAs exhibit distinct regional distributions in the mouse brain. Colocalization of CB1R and MOR was primarily observed in the paraventricular nucleus of the thalamus (PVT), where ~50% of vesicular glutamate transporter 2 (Vglut2)-positive glutamatergic neurons displayed CB1R-MOR co-expression. In contrast, only a small subset (5%-25%) of Vglut2-positive neurons in pain-related regions, such as the periaqueductal gray (PAG) and the dorsal horn of the spinal cord, or vesicular GABA transporter (Vgat)-positive GABA neurons in reward-related regions, such as the nucleus accumbens, ventral tegmental area, and substantia nigra, exhibited such colocalization. Unexpectedly, the selective deletion of MOR from Vglut2-positive glutamatergic neurons or Vgat-positive GABAergic neurons did not alter the effects of Δ
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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.