iBet uBet web content aggregator. Adding the entire web to your favor.
iBet uBet web content aggregator. Adding the entire web to your favor.



Link to original content: https://pubmed.ncbi.nlm.nih.gov/23863631
Chronic THC intake modifies fundamental cerebellar functions - PubMed Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Comment
. 2013 Aug;123(8):3208-10.
doi: 10.1172/JCI70226.

Chronic THC intake modifies fundamental cerebellar functions

Affiliations
Comment

Chronic THC intake modifies fundamental cerebellar functions

Nephi Stella. J Clin Invest. 2013 Aug.

Abstract

Delta9-tetrahydrocannabinol (THC), the principal bioactive component in the Cannabis plant, is truly a captivating drug. Acute and chronic THC intake produces a spectrum of biological effects ranging from transient psychotropic effects to prolonged medicinal benefits, many of which have been fostered for centuries by our society. In the July 2013 issue of the JCI, Cutando et al. combined mouse genetics with classic mouse behavioral analysis to deepen our understanding of the physiological consequence of subchronic THC intake on eyeblink reflexes, a fundamental neuronal adaptive response, revealing that this regimen leads to downregulation of the cannabinoid CB1 receptor (referred to as CB1 in the Cutando et al. article) in cerebellar stress fibers and the activation of microglia, raising provocative new questions about the safety profile of regimented THC intake.

PubMed Disclaimer

Figures

Figure 1
Figure 1. In mice, subchronic treatment with THC leads to the downregulation of presynaptic cannabinoid CB1 receptors expressed by parallel fibers that project onto Purkinje cells.
Cutando et al. (9) show that the loss of CB1 receptors, either due to TCH-induced downregulation or genetic deletion, triggers a neuroinflammatory response typified by changes in microglial cell morphology and CB2 receptor expression. This adaptive response underlies THC-induced deficits in cerebellar-associated learning functions.

Comment on

Similar articles

Cited by

References

    1. Matsuda LA, Lolait SJ, Brownstein MJ, Young AC, Bonner TI. Structure of a cannabinoid receptor and functional expression of the cloned cDNA. Nature. 1990;346(6284):561–564. doi: 10.1038/346561a0. - DOI - PubMed
    1. Steindel F, et al. Neuron-type specific cannabinoid-mediated G protein signalling in mouse hippocampus. J Neurochem. 2013;124(6):795–807. doi: 10.1111/jnc.12137. - DOI - PubMed
    1. Berghuis P, et al. Hardwiring the brain: endocannabinoids shape neuronal connectivity. Science. 2007;316(5828):1212–1216. doi: 10.1126/science.1137406. - DOI - PubMed
    1. Katona I, Freund TF. Endocannabinoid signaling as a synaptic circuit breaker in neurological disease. Nat Med. 2008;14(9):923–930. doi: 10.1038/nm.f.1869. - DOI - PubMed
    1. Kreitzer AC, Malenka RC. Endocannabinoid-mediated rescue of striatal LTD and motor deficits in Parkinson’s disease models. Nature. 2007;445(7128):643–647. doi: 10.1038/nature05506. - DOI - PubMed

Publication types