Cannabis er godt for hjernen
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Cannabinoids promote embryonic and adult hippocampus neurogenesis and produce anxiolytic- and antidepressant-like effects
ArtikelThe hippocampal dentate gyrus in the adult mammalian brain contains neural stem/progenitor cells (NS/PCs) capable of generating new neurons, i.e., neurogenesis. Most drugs of abuse examined to date decrease adult hippocampal neurogenesis, but the effects of cannabis (marijuana or cannabinoids) on hippocampal neurogenesis remain unknown. This study aimed at investigating the potential regulatory capacity of the potent synthetic cannabinoid HU210 on hippocampal neurogenesis and its possible correlation with behavioral change.
The recent discovery that the hippocampus is able to generate new neurons (i.e., neurogenesis) throughout the lifespan of mammals, including humans, has changed the way we think about the mechanisms of psychiatric disorders (12) and drug addiction (13). The subgranular zone of the dentate gyrus (SGZ) in the adult brain contains neural stem/progenitor cells (NS/PCs) capable of producing thousands of new granule cells per day (14). We, and others, have shown that these newborn hippocampal neurons are functionally integrated into the existing neuroanatomical circuitry (15, 16) and are positively correlated with hippocampus-dependent learning and memory processes (17) and the developmental mechanisms of stress and mood disorders (12). Recent studies have further shown that chronic fluoxetine treatment produced antidepressant and anxiolytic effects (18, 19) and the anxiolytic effects are likely achieved by promoting hippocampal neurogenesis (18).
Although both HU210 and AEA exerted no significant effects on neuronal differentiation of NS/PCs, they significantly increased NS/PC proliferation, leading to increased total number of newborn neurons. Similar results were also obtained in freely moving adult rats. That is, chronic, but not acute, HU210 significantly increased the number of newborn hippocampal neurons in adult rats by promoting NS/PC proliferation but not differentiation. We also provided evidence indicating that the promoting effects of chronic HU210 treatment on adult hippocampal neurogenesis are not the outcome of hippocampal neuronal death, as we did not detect neuronal loss or dying hippocampal neurons following chronic HU210 injection. Overall, these data support the idea that cannabinoids are able to promote embryonic and adult hippocampal neurogenesis via the CB1 receptors in the NS/PCs.
Following the observation that chronic HU210 treatment promoted neurogenesis in the dentate gyrus, we wondered whether chronic HU210–induced newborn neurons are of functional significance. Given the recent findings that chronic fluoxetine treatment produced antidepressant and anxiolytic effects (18, 19) and the anxiolytic effects are likely achieved by promoting hippocampal neurogenesis (18), we hypothesized that chronic HU210–induced hippocampal neurogenesis may also correlate with anxiolytic and antidepressant effects. Our subsequent experiments supported this hypothesis. After 1 month of chronic HU210 treatment, rats deprived of food for 48 hours showed significantly reduced latency to eat food in a novel environment, suggesting that chronic HU210 treatment exerted anxiolytic effects.
One week after undergoing NSF testing, the same rats receiving chronic HU210 treatment showed a significantly reduced duration of immobility in the FST, indicating that chronic HU210 also exerts antidepressant effects. Because acute cannabinoid treatment profoundly affects motor function of humans and animals (1, 10), chronic HU210–induced shortened immobility in the FST may be produced by its action in changing the motor activity of rats. This is unlikely, however, as we observed no significant difference in the number of rats climbing (41, 42) among HU210-, AM281-, and vehicle-treated groups in the first 5 minutes of the pretest sessions of the FST. The anxiolytic- and antidepressant-like behavioral changes in rats 1 month after chronic HU210 treatment are unlikely to have been produced by the cannabinoid withdrawal effects, since, as shown in our recent study (8), rodents receiving chronic cannabinoid would display detectable cannabinoid withdrawal syndrome only after administration of CB1 receptor antagonists.
Finally, the same rats with reduced measures of anxiety and depression following chronic HU210 treatment showed significantly increased numbers of BrdU-labeled cells within the dentate granule cell layer. These overall results thus confirmed our above-described novel findings that chronic HU210 treatment significantly increased newborn neurons in the hippocampal dentate gyrus (Figure 6).
In summary, since adult hippocampal neurogenesis is suppressed following chronic administration of opiates (20), alcohol (21), nicotine (22), and cocaine (23), the present study suggests that cannabinoids are the only illicit drug that can promote adult hippocampal neurogenesis following chronic administration. Increased hippocampal neurogenesis appears to underlie the mechanism of anxiolytic- and antidepressant-like effects produced by a high dose of chronic HU210 treatment. The opposing effects of high doses of acute and chronic cannabinoids, together with the anxiolytic-like effects caused by a low dose of cannabinoids, may finally explain discrepancies in the clinical study literature regarding the effects of cannabinoid on anxiety and depression.
Summasummarum: Cannabis forstærker neurogenesis, hvilket kort sagt resulterer i forbedret hukommelse/indlæring og humør.
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