Cannabigerol (CBG) prevented long-term memory impairment in a model of schizophrenia, according to a new study being published in the upcoming issue of the journal Pharmacology Biochemistry and Behavior, and published online ahead of print by the U.S. National Library of Medicine.
The research was conducted by scientists from the Instituto de Investigaciones Biológicas Clemente Estable and Universidad de la República in Uruguay, along with researchers affiliated with Phytoplant Research S.L., Universitat de Vic–Universitat Central de Catalunya, the University of Barcelona and Spain’s Biomedical Research Networking Center in Mental Health.
Researchers said interest in CBG, a non-intoxicating cannabinoid found in marijuana, has increased because of its potential therapeutic properties, while noting that “preclinical studies examining its effects on cognitive impairment, a core symptom domain of schizophrenia, remain limited.”
For the study, researchers used male rats treated with MK-801, a drug that blocks N-methyl-D-aspartate (NMDA) receptors and is commonly used in animal research to reproduce certain cognitive impairments associated with schizophrenia.
Rats received a single 0.1 mg/kg dose of MK-801, while CBG was administered repeatedly at 10 mg/kg. Researchers then evaluated long-term recognition memory using the novel object recognition test, which measures whether animals can distinguish between previously encountered and new objects.
MK-801 significantly impaired long-term memory compared with the control group. However, animals receiving CBG alongside MK-801 did not experience the same memory deficit, with researchers finding that CBG “prevented this deficit.”
The researchers also examined brain-derived neurotrophic factor (BDNF) and its TrkB receptor, a signaling system involved in learning, memory and neuronal function.
MK-801 reduced BDNF protein levels in both the hippocampus and medial prefrontal cortex, two brain regions important for memory and cognition. CBG did not restore those BDNF levels, but the combined CBG and MK-801 treatment significantly increased TrkB receptor gene expression in the medial prefrontal cortex.
Researchers said the finding suggests CBG’s protective effect on memory may involve activation of TrkB receptor signaling through a mechanism that does not depend directly on BDNF.
They conclude the study by stating “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.”
