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Published on: August 1, 2025
β-caryophyllene, a CB2-selective phytocannabinoid, differentially modulates attention and inhibitory control in low-
Williams M N1, Patel N T1, Fleischel E J2
1Department of Psychology and Neuroscience, Temple University, 1701 N. 13th Street, Philadelphia, PA, 19122, USA.
Rationale:
Evidence suggests that modulation of cannabinoid signaling via CB2 receptors regulates neuroinflammation and confers neuroprotection, positioning these receptors as promising targets for age-related cognitive decline. However, there are limited studies that have directly explored the effects of acute CB2 receptor activation on cognitive domains impacted in aging.
Objective:
This study examined the impact of β-caryophyllene (BCP), a sesquiterpene with putative CB2 receptor agonist properties, on executive function and recognition memory in young and aged mice.
Methods:
Young (2 mo) and aged (15 mo) male and female C57BL/6J mice were trained in an operant go/no-go (GNG) visual discrimination task. Animals trained to criterion were injected with BCP (0, 25, 50, or 100 mg/kg; i.p.) using a within-subjects design. BCP effects were also tested in novel object recognition (NOR) and object location recognition (OLR) paradigms.
Results:
Aged mice required more sessions than young mice to acquire GNG contingencies but performed equivalently post-acquisition. Acute BCP induced dose-dependent impairments in attentional control, with moderate-to-high doses (50 and 100 mg/kg) reducing go trial performance independent of age or sex, while inhibitory control (no-go trial performance) remained unaffected. In contrast, low-dose BCP (25 mg/kg) selectively enhanced inhibitory control in aged low-performing mice but not in young or high-performing aged mice. Low-dose BCP improved NOR but not OLR performance.
Conclusions:
Acute BCP produces domain- and dose-specific cognitive effects, with low doses enhancing inhibitory control in cognitively vulnerable aged mice. These rapid effects likely arise from neuromodulatory rather than delayed anti-inflammatory mechanisms, warranting further validation of CB2 receptor dependence.
