Neuroscience 2001 Abstract
| Presentation Number: | 109.13 |
|---|---|
| Abstract Title: | Neuroprotective properties of cannabinoids in vitro: role of the cannabinoid receptor CB1. |
| Authors: |
Lutz, B.*1
; Marsicano, G.1
; Moosmann, B.1
; Hermann, H.1
; Behl, C.1
1Max-Planck-Institute of Psychiatry, Munich, Germany |
| Primary Theme and Topics |
Neurological and Psychiatric Conditions - Neurotoxicity -- Apoptosis |
| Secondary Theme and Topics | Synaptic Transmission and Excitability<br />- Neurotransmitters<br />-- Cannabinoids |
| Session: |
109. Neurotoxicity: apoptosis II Poster |
| Presentation Time: | Sunday, November 11, 2001 8:00 AM-9:00 AM |
| Location: | Exhibit Hall AAA-14 |
| Keywords: | cannabinoids, neuroprotection, knockout, oxidative stress |
Neuroprotective effects have been described for many cannabinoids in several neurotoxicity models. However, the exact mechanisms have not been clearly understood yet. In the present study, antioxidant neuroprotective effects of cannabinoids and the involvement of the cannabinoid receptor 1 (CB1) were analyzed employing cell-free biochemical assays and cultured cells. As it was reported for estrogens that the phenolic group is a lead structure for antioxidant neuroprotective effects, the nine compounds tested were classified into three groups. Group A: phenolic compounds not binding to CB1 (cannabinol, cannabidiol, AM 404). Group B: non-phenolic compounds binding to CB1 (methanandamide, WIN 55,212-2, SR 141716A). Group C: phenolic compounds binding to CB1 (D9-THC, CP 55,940, HU 210). In the biochemical assays employed, a requirement of the phenolic lead structure for antioxidant activity was shown. The effects paralleled the protective potential of group A and C compounds in oxidative neuronal cell death using the mouse hippocampal HT22 cell line and rat primary cerebellar cultures. To study the role of CB1 in neuroprotection, we established stably transfected HT22 cell clones containing CB1 and compared the protection potential of cannabinoids with that one observed in the control HT22 cells. Furthermore, oxidative stress experiments were performed in cultured cerebellar granule cells, which were derived either from CB1 knockout mice or from wild-type littermates. The results suggest that CB1 is not involved in the in vitro antioxidant neuroprotective effects of cannabinoids.
Supported by Deutsche Forschungsgemeinschaft and Alzheimer Forschung Initiative e.V.
Sample Citation:
[Authors]. [Abstract Title]. Program No. XXX.XX. 2001 Neuroscience Meeting Planner. San Diego, CA: Society for Neuroscience, 2001. Online.
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