What topics does this cannabis study cover?

This study covers research on: Pain, Inflammation, Endocannabinoid.

Where was this research published?

Published in Behavioural brain research on June 11, 2026.

FAAH inhibition reduced inflammatory pain in mice, with opioid links

Q: What did this research study find?

In a *mouse model* of persistent inflammatory pain, the FAAH inhibitor PF3845 **reduced nociception and pain aversion**.

Fatty acid amide hydrolase (FAAH) inhibitor reduces persistent inflammatory pain in mice depending on μ- and δ-opioid receptors activity: Involvement of heme oxygenase-1.

Behavioural brain research • June 11, 2026 • Highly Relevant

🤖

AI Summary

This animal study asked whether blocking fatty acid amide hydrolase (FAAH)—thereby activating the endocannabinoid system—could reduce persistent inflammatory pain in male BALB/c mice. The mice received a paw injection of CFA to produce ongoing inflammation and were treated with the FAAH inhibitor PF3845 or the heme oxygenase-1 (HO-1) inducer CoPP. Both treatments reduced pain-related responses and pain aversion. The abstract does not report quantitative results such as sample sizes or effect sizes.

The effects of PF3845 and CoPP were blocked by an HO-1 inhibitor and by antagonists of μ-opioid and δ-opioid receptors, suggesting that these systems may contribute to the observed responses. PF3845 also increased HO-1 levels and prevented an increase in microglial expression in the basolateral amygdala. Because this was a mouse study, and the abstract notes that the relevant supraspinal circuits require further investigation, it cannot establish that FAAH inhibition would relieve pain in people or prove the precise causal pathway. This is an abstract-based summary; the full text was not reviewed.

💡 Key Findings

In a mouse model of persistent inflammatory pain, the FAAH inhibitor PF3845 reduced nociception and pain aversion.

Good

60%

The pain-related effects of PF3845 and the HO-1 inducer CoPP were blocked by inhibitors or antagonists targeting HO-1, μ-opioid receptors, and δ-opioid receptors, suggesting involvement of these systems.

Moderate

58%

PF3845 increased HO-1 levels and prevented increased microglial expression in the basolateral amygdala; the abstract identifies these brain-circuit findings as mechanistic leads requiring further study.

Moderate

52%

📄 Original Abstract

The endocannabinoid system modulates chronic pain, and its actions in the nervous system may involve interactions with other systems. We aimed to investigate the effect of activating the endocannabinoid system by inhibiting fatty acid amide hydrolase (FAAH) on persistent inflammatory pain, as well as its interactions with heme oxygenase 1 (HO-1) and μ-opioid receptors (MOR) and δ-opioid receptors (DOR). Male BALB/c mice submitted to persistent inflammatory pain through intra-plantar injection of CFA were treated with a FAAH inhibitor (PF3845) or an HO-1 inducer (CoPP), combined with an HO-1 inhibitor (SnPP), a MOR antagonist (CTAP), or a DOR antagonist (naltrindole). PF3845 and CoPP reduced nociception and pain aversion, and this effect was blocked by SnPP, CTAP, and Naltrindole. PF3845 decreased FAAH and increased HO-1 levels in the amygdala and prevented microglial expression increase in the basolateral amygdala. This study highlights FAAH inhibition as a relevant mechanism for modulating persistent pain, potentially involving MOR, DOR, and HO-1 activity. Supraspinal circuits, including amygdala nuclei, may be relevant to the development and reduction of pain aversion by FAAH inhibitors and require further investigation to determine causal relationships.

Paper Type

📄 Research

Publication

Journal: Behavioural brain research
Published: June 11, 2026
PMID: 42276284
DOI: 10.1016/j.bbr.2026.116329

Authors (4)

Vítor Pansarim Psychology Department, Faculty of Philosophy, Sciences, and Letters at Ribeirão Preto, University of São Paulo, Ribeirão Preto, SP, Brazil.
Aline A Ferrarese-Tiballi Psychology Department, Faculty of Philosophy, Sciences, and Letters at Ribeirão Preto, University of São Paulo, Ribeirão Preto, SP, Brazil.
Olga Pol Grup de Neurofarmacologia Molecular, Institut de Recerca Sant Pau, Barcelona 08041, Spain; Institut de Neurociències, Universitat Autònoma de Barcelona, Barcelona 08193, Spain.
Christie Leite-Panissi Psychology Department, Faculty of Philosophy, Sciences, and Letters at Ribeirão Preto, University of São Paulo, Ribeirão Preto, SP, Brazil. Electronic address: christie@usp.br.

MeSH Keywords

Animals Fatty Acid Amide Hydrolases Male Amidohydrolases Receptors, Opioid, delta Mice Heme Oxygenase-1 Receptors, Opioid, mu Mice, Inbred BALB C Inflammation +8 more