
Cannabigerol (CBG) is gaining attention for its potential effects on brain function, including memory and cognition.
In this animal study, researchers found that CBG improved a long-term recognition memory deficit induced by MK-801 in male rats. The effect was linked to TrkB receptor signaling in the cortex and appeared to occur independently of changes in BDNF levels.
The findings add to emerging research on CBG’s neurological effects and suggest a potential role in pathways involved in memory impairment.
“Interest in the therapeutic potential of cannabigerol (CBG), a non-psychotomimetic cannabinoid derived from Cannabis sativa, has increased recently. However, preclinical studies examining its effects on cognitive impairment, a core symptom domain of schizophrenia, remain limited.
Based on the N-methyl-d-aspartate receptor (NMDA-R) hypofunction hypothesis of schizophrenia, MK-801, a potent NMDA-R antagonist, is widely used as a pharmacological model of schizophrenia that replicates the cognitive impairments observed in patients.
This study investigated whether repeated systemic administration of CBG (10 mg/kg/i.p.) could reverse long-term recognition memory (LTM) impairment induced by a single dose of MK-801 (0.1 mg/kg/i.p.) in male rats, using the novel object recognition paradigm. Additionally, we evaluated whether these effects were associated with changes in BDNF/TrkB receptor (TrkB-R) signaling.
ELISA and quantitative real-time PCR analyses were performed to evaluate BDNF protein levels and BDNF and TrkB-R mRNA expression in the hippocampus and medial prefrontal cortex (mPFC).
MK-801 significantly impaired LTM compared with control group, whereas co-administration of CBG prevented this deficit.
MK-801-induced memory impairment was associated with reduced hippocampal and cortical BDNF protein levels, without changes in BDNF or TrkB-R mRNA expression. CBG and MK-801 combined treatment did not restore BDNF mRNA expression and protein levels although it significantly increased TrkB-R mRNA expression in the mPFC.
These results suggest that activation of TrkB-R signaling through a BDNF-independent mechanism may contribute to the preservation of LTM by CBG.
Our results provide relevant evidence supporting the therapeutic potential of CBG for cognitive impairments associated with schizophrenia.”
https://pubmed.ncbi.nlm.nih.gov/42648374
“Results support CBG therapeutic potential for cognitive impairments in patients with schizophrenia.”
https://www.sciencedirect.com/science/article/abs/pii/S0091305726001152?via%3Dihub










