Neuroscience 2001 Abstract
| Presentation Number: | 805.4 |
|---|---|
| Abstract Title: | CANNABINOID-INDUCED ASTROTOXICITY. |
| Authors: |
Jeremic, A. M.*1
; Jeftinija, K.1
; Glavaski, A.1
; Stevanovich-Popovich, J.1
; Jeftinija, S.1
1Biomed Sci, Iowa State Univ, Ames, IA |
| Primary Theme and Topics |
Synaptic Transmission and Excitability - Neurotransmitters -- Cannabinoids |
| Secondary Theme and Topics | Neurological and Psychiatric Conditions<br />- Neurotoxicity<br />-- Apoptosis |
| Session: |
805. Neurotransmitters: cannabinoids Poster |
| Presentation Time: | Wednesday, November 14, 2001 4:00 PM-5:00 PM |
| Location: | Exhibit Hall D-28 |
| Keywords: | cannabinoids, calcium, neurotoxicity, apoptosis |
The effect of cannabinoids on calcium transients and the cell viability in astrocyte culture were studied. Both THC and Win 55,212-2 (WIN) induced decrease in the cell viability and raised [Ca2+]i in a dose-dependent manner. Threshold concentration was 1 and 10 μM, respectively. Cannabinoids (10 μM) produced a biphasic response in [Ca2+]i; a rapid change in [Ca2+]i was followed by a slow/delayed irreversible increase in [Ca2+]i. The delayed, irreversible calcium elevation was accompanied with the cell loss at the end of the experiment. Exposure of the cultures to 2.5 μM THC in duration of 24 hours produced a massive disintegration in astrocyte cultures. SR-141716A, a CB1 receptor antagonist blocked both THC stimulatory effects on Ca2+ transients and THC-induced astrotoxicity. PTX pretreatment abrogated THC toxic effect pointing to the role of Gi protein in signaling mechanism. PKC and ERK kinase inhibitors significantly (p<0.001,n=8) protected astrocytes against THC toxicity. Actinomycin D, an inhibitor of transcription, abrogated the THC-induced astrotoxicity suggesting that cannabinoids may activate a transcription-dependent cell death. In addition, antioxidants vitamin E and N-acetyl-cysteine were able to antagonize THC toxicity supporting the role of radicals. These data demonstrate a previously unknown property for astroglia in induction of cannabinoid-mediated astrotoxicity, show that neurotoxicity can be initiated by nonneuronal signals, and raise the possibility that astroglia may actively participate in neurotoxicity of cannabinoids.
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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