St8sia2 deficiency plus juvenile cannabis exposure in mice synergistically affect higher cognition in adulthood.
Martesa Tantra, Tim Kröcher, Sergi Papiol, Daniela Winkler, Iris Röckle, Jasmin Jatho, Hannelore Burkhardt, Anja Ronnenberg, Rita Gerardy-Schahn, Hannelore Ehrenreich, Herbert Hildebrandt
Behavioural Brain Research December 15, 2014 DOI: 10.1016/j.bbr.2014.08.062 (opens in new tab)
Study at a glance
AI-extracted from the abstract| Characteristics | Animal experimental study Peer reviewed |
|---|---|
| Population | Juvenile male St8sia2 knockout and wildtype mice |
| Intervention | Delta-9-tetrahydrocannabinol (Δ9-THC) |
| Dose | 7 mg/kg every other day |
| Duration | 3 weeks of treatment, with effects assessed months after the last dose |
| Topics | Cannabis |
| Keywords | Learning index Ncam Polysia Reference memory Working memory δ-9-THC |
| Key findings | Chronic juvenile Δ9-THC treatment produced synergistic, delayed cognitive impairment in St8sia2 knockout mice but not wildtype mice. The deficits appeared months after the last dose and were accompanied by changes in hippocampal NCAM polysialylation. The authors conclude that adolescent cannabis exposure may cause lasting cognitive damage in genetically predisposed subjects. |
Abstract
The neural cell adhesion molecule (NCAM) and its functionally linked polysialyltransferases, ST8SIA2 and ST8SIA4, are crucial for synaptic plasticity. Variations in encoding genes have been associated with mental illness. Since cannabinoids can alter NCAM polysialylation, we hypothesized that delta-9-tetrahydrocannabinol (Δ9-THC) might act as environmental 'second hit' regarding cognition of St8sia2(-/-) mice. These mice show per se minor behavioral abnormalities, consisting of reduced anxiety and mild cognitive deficits. Chronic Δ9-THC treatment of juvenile male wildtype mice (St8sia2(+/+)) (7mg/kg every other day over 3 weeks) did not appreciably affect cognition. St8sia2(-/-) mice, however, displayed a synergistic negative consequence of Δ9-THC on learning/memory, accompanied by polysialic acid-free NCAM-180 reduction in hippocampus and polysialic acid increase in dentate outer molecular layer. These synergistic effects became obvious only months after the last Δ9-THC. We conclude that juvenile cannabis exposure may cause delayed but lasting damage on cognition in subjects genetically predisposed to altered NCAM polysialylation.
Comparable studies
Other preclinical and animal studies on cannabis, most cited first.
Citations in the library
Cited by 2
- Adolescent Δ9-Tetrahydrocannabinol Exposure and Astrocyte-Specific Genetic Vulnerability Converge on Nuclear Factor-κB-Cyclooxygenase-2 Signaling to Impair Memory in Adulthood. Biological Psychiatry August 16, 2018
- Adolescent cannabis exposure interacts with mutant DISC1 to produce impaired adult emotional memory. Neurobiology of Disease October 2015
Cites 6
- Adolescent cannabis use and psychosis: epidemiology and neurodevelopmental models British Journal of Pharmacology June 1, 2010
- Puberty as a highly vulnerable developmental period for the consequences of cannabis exposure. Addiction Biology June 2008
- Acute activation of CB1 cannabinoid receptors transiently decreases PSA-NCAM expression in the dentate gyrus of the rat hippocampus. Brain Research May 7, 2007
- Acute marijuana effects on human risk taking. Neuropsychopharmacology April 2005
- Endocannabinoid signaling in the brain. Science April 26, 2002
and 1 more in the library