Neuroscience 2005 Abstract
| Presentation Number: | 755.1 |
|---|---|
| Abstract Title: | Modulation of δ9-THC-induced ataxia by mouse cerebellar nicotinic--cholinergic receptor subtype. |
| Authors: |
Smith, A. D.*1
; Dar, M.1
1Pharmacology & Toxicology, ECU-Brody School of Medicine, Greenville, NC |
| Primary Theme and Topics |
Sensory and Motor Systems - Cerebellum -- Cortex and nuclei |
| Session: |
755. Anatomy and Pathology Poster |
| Presentation Time: | Tuesday, November 15, 2005 1:00 PM-2:00 PM |
| Location: | Washington Convention Center - Hall A-C, Board # FF18 |
| Keywords: |
No study regarding effects of Δ9-THC and nicotine co-administration on motor functions is known. Therefore, it was interesting to investigate functional consequences of intracerebellar (ICB) microinfusion of nicotine on ICB Δ9-THC-induced ataxia. Cerebellum was selected because of its established role in Δ9-THC-induced ataxia. Using the Rotorod, the effect of direct ICB microinfusion of various doses of nicotine [5, 2.5,1.25ng] on Δ9-THC [20 µg]-induced ataxia was investigated. There was a significant (p<0.05) attenuation by ICB nicotine on Δ9-THC-induced ataxia in a dose-related manner. The highest nicotine dose (5 ng) virtually abolished the Δ9-THC-induced ataxia. ICB pretreatment with nicotine antagonist hexamethonium (1µg) significantly blocked nicotine’s ability to attenuate Δ9-THC-induced ataxia suggesting that a nicotine - Δ9-THC behavioral interaction involved participation of nAChR. To further elucidate specific subtype of nicotinic receptor involved in the attenuation of Δ9-THC-induced ataxia, direct ICB microinfusion of RJR-2403 [750, 500, 250ng], a selective α4β2 nicotinic receptor agonist, significantly (p<0.05) attenuated Δ9-THC-induced ataxia in a dose-related manner, with the highest RJR-2403 dose (750 ng) virtually abolishing Δ9-THC-induced ataxia. ICB DHβE [750ng], a selective α4β2 antagonist, virtually abolished both nicotine and RJR-2403’s ability to attenuate Δ9-THC-induced ataxia, thus further identifying the α4β2 receptor’s role in modulating Δ9-THC-induced ataxia. In contrast, the α7 nicotinic receptor subtype antagonist, MLA [1µg] had no effect in the attenuation of Δ9-THC-induced ataxia in the presence of either nicotine or RJR-2403, further indicating role of α4β2 and not α7 subtype in modulating Δ9-THC-induced ataxia. The results of the present investigation support a possible role of α4β2 subtype of cerebellar nicotinic-cholinergic receptor in the modulation of Δ9-THC-induced cerebellar ataxia.
Sample Citation:
[Authors]. [Abstract Title]. Program No. XXX.XX. 2005 Neuroscience Meeting Planner. Washington, DC: Society for Neuroscience, 2005. Online.
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