BMC genomics · 2026
Selective hippocampal transcriptional adaptation to long-term cannabidiol exposure in mice.
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Żurowski J, Ocłoń E, Jasielczuk I, Szmatoła T, Mizera-Szpilka K, Taubner T, Szumiec L, Semik-Gurgul E, Gurgul A
Аннотация
BACKGROUND: CBD is widely studied for its stress-reduction and cognitive-enhancing properties, but its effects on hippocampal molecular organisation under physiological settings are unknown. Acute and long-term intraperitoneal CBD treatment at different doses was tested on hippocampus gene expression, circulating corticosterone, and behavioural performance in C57BL/6J mice.
RESULTS: Short-term administration did not induce detectable transcriptional changes. In contrast, long-term treatment with 10 mg/kg CBD, but not lower or higher doses, resulted in significant hippocampal transcriptional remodelling. Overrepresentation analysis showed coordinated control of mitochondrial oxidative phosphorylation genes, particularly numerous respiratory chain complex I components, and purine and nucleotide metabolic pathways. Shared mitochondrial respiratory genes, not classical disease-associated effectors, enriched KEGG categories for neurodegeneration and retrograde endocannabinoid signalling. The endocrine profile showed a temporary increase in circulating corticosterone after short-term exposure, but long-term dosing decreased it. Behavioural effects were modest and limited across paradigms.
CONCLUSIONS: These results show that long-term administration of an intermediate CBD dose alters subsets of genes related to coordinated bioenergetic and nucleotide-related transcriptional adaptation in the hippocampus, which modulates endocrine stress markers but does not disrupt behaviour. The data suggest that chronic CBD exposure may cause metabolic recalibration in stress-sensitive brain circuits rather than acute neuromolecular reprogramming.
RESULTS: Short-term administration did not induce detectable transcriptional changes. In contrast, long-term treatment with 10 mg/kg CBD, but not lower or higher doses, resulted in significant hippocampal transcriptional remodelling. Overrepresentation analysis showed coordinated control of mitochondrial oxidative phosphorylation genes, particularly numerous respiratory chain complex I components, and purine and nucleotide metabolic pathways. Shared mitochondrial respiratory genes, not classical disease-associated effectors, enriched KEGG categories for neurodegeneration and retrograde endocannabinoid signalling. The endocrine profile showed a temporary increase in circulating corticosterone after short-term exposure, but long-term dosing decreased it. Behavioural effects were modest and limited across paradigms.
CONCLUSIONS: These results show that long-term administration of an intermediate CBD dose alters subsets of genes related to coordinated bioenergetic and nucleotide-related transcriptional adaptation in the hippocampus, which modulates endocrine stress markers but does not disrupt behaviour. The data suggest that chronic CBD exposure may cause metabolic recalibration in stress-sensitive brain circuits rather than acute neuromolecular reprogramming.