CoChat
Sign Up
Cited by 407Cannabis and Cannabinoid ResearchParkinson's Disease Mechanisms and TreatmentsAlzheimer's disease research and treatments

The DOI matches its Crossref record; 106 of the 108 references it cites were found in a registry or an index.

Cannabinoids provide neuroprotection against 6-hydroxydopamine toxicity in vivo and in vitro: Relevance to Parkinson's disease

Open access
Lastres-Becker, Isabel, Molina-Holgado, Francisco, Ramos, José A., Mechoulam, Raphael, Fernández-Ruiz, Javier·2005·Neurobiology of Disease
DOI 10.1016/j.nbd.2004.11.009
Open this paper in CoChat — free account

Abstract

Cannabinoids have been reported to provide neuroprotection in acute and chronic neurodegeneration. In this study, we examined whether they are also effective against the toxicity caused by 6-hydroxydopamine, both in vivo and in vitro, which may be relevant to Parkinson's disease (PD). First, we evaluated whether the administration of cannabinoids in vivo reduces the neurodegeneration produced by a unilateral injection of 6-hydroxydopamine into the medial forebrain bundle. As expected, 2 weeks after the application of this toxin, a significant depletion of dopamine contents and a reduction of tyrosine hydroxylase activity in the lesioned striatum were noted, and were accompanied by a reduction in tyrosine hydroxylase-mRNA levels in the substantia nigra. None of these events occurred in the contralateral structures. Daily administration of delta9-tetrahydrocannabinol (delta9-THC) during these 2 weeks produced a significant waning in the magnitude of these reductions, whereas it failed to affect dopaminergic parameters in the contralateral structures. This effect of delta9-THC appeared to be irreversible since interruption of the daily administration of this cannabinoid after the 2-week period did not lead to the re-initiation of the 6-hydroxydopamine-induced neurodegeneration. In addition, the fact that the same neuroprotective effect was also produced by cannabidiol (CBD), another plant-derived cannabinoid with negligible affinity for cannabinoid CB1 receptors, suggests that the antioxidant properties of both compounds, which are cannabinoid receptor-independent, might be involved in these in vivo effects, although an alternative might be that the neuroprotection exerted by both compounds might be due to their anti-inflammatory potential. As a second objective, we examined whether cannabinoids also provide neuroprotection against the in vitro toxicity of 6-hydroxydopamine. We found that the non-selective cannabinoid agonist HU-210 increased cell survival in cultures of mouse cerebellar granule cells exposed to this toxin. However, this effect was significantly lesser when the cannabinoid was directly added to neuronal cultures than when these cultures were exposed to conditioned medium obtained from mixed glial cell cultures treated with HU-210, suggesting that the cannabinoid exerted its major protective effect by regulating glial influence to neurons. In summary, our results support the view of a potential neuroprotective action of cannabinoids against the in vivo and in vitro toxicity of 6-hydroxydopamine, which might be relevant for PD. Our data indicated that these neuroprotective effects might be due, among others, to the antioxidant properties of certain plant-derived cannabinoids, or exerted through the capability of cannabinoid agonists to modulate glial function, or produced by a combination of both mechanisms.

Overview

Integrity signals

Registry

Crossref · 10.1016/j.nbd.2004.11.009

Cites

106 of 106 references verified0 citation errors · 0 not checkable

Statistics

Recomputing p-values needs the paper’s full text.

Verification

Claims the paper makes

We couldn’t retrieve this paper’s full text, so its claims and self-check weren’t run. The registry and citation checks still apply.

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

Citations

Cites

Flagged first, then by citations

Show all 108 references

2 of the 108 references couldn’t be matched to a known paper.

Cited by

Sorted by citations

Items 301–400 of 405

Related

See all

Metadata

Authors
Lastres-Becker, I., Molina-Holgado, F., Ramos, J. A., Mechoulam, R., & Fernández-Ruiz, J.
Affiliations
  • Universidad Complutense de Madrid (ES)
  • Hebrew University of Jerusalem (IL)
ORCID
Venue
Neurobiology of Disease
Publisher
Elsevier BV
Published
2005-06
Volume
19
Issue
1-2
Pages
96-107
ISSN
0969-9961 (ISSN-L)
DOI
10.1016/j.nbd.2004.11.009
OpenAlex
W2110514788
Cited by
407
References
108
Citations by year
2026: 8 · 2025: 13 · 2024: 23 · 2023: 25 · 2022: 23 · 2021: 30 · 2020: 29 · 2019: 26 · 2018: 15 · 2017: 26 · 2016: 20 · 2015: 13 · 2014: 13 · 2013: 14 · 2012: 16
FWCI
12.12
Type
journal article
Language
en
Open access
Licence
Locations
  • Neurobiology of Disease (publishedVersion)
  • PubMed (publishedVersion)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
  • Research Portal (King's College London) (submittedVersion)
Funders
Deakin University
Topics
  • Health Sciences › Medicine › Pharmacology (medical) › Cannabis and Cannabinoid Research
  • Health Sciences › Medicine › Clinical Neurology › Parkinson's Disease Mechanisms and Treatments
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
Keywords
cannabinoids, neuroprotection, 6-hydroxydopamine, Parkinson's disease, delta-9-tetrahydrocannabinol, cannabidiol, HU-210, dopamine depletion, tyrosine hydroxylase, substantia nigra, striatum, neuron-glia interactions, cerebellar granule cells
MeSH terms
Animals, Cannabinoids, Cell Survival, Cells, Cultured, Dopamine, Male, Mice, Inbred C57BL, Parkinson Disease, Oxidopamine, Rats, Sprague-Dawley, Neuroprotective Agents, Mice, Rats

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review