Neuroscience 2004 Abstract
| Presentation Number: | 58.4 |
|---|---|
| Abstract Title: | How endocannabinoid-mediated long-term depression responds to single and chronic in-vivo exposure to Δ-9-Tetrahydrocannabinol. |
| Authors: |
Mato, S.*1
; Manzoni, O. J. J.2
1Institut Magendie des Neurosciences, INSERM, 33077 Bordeaux Cedex, France 2Equipe Avenir, INSERM, 33077 Bordeaux Cedex, France |
| Primary Theme and Topics |
Synaptic Transmission and Excitability - Synaptic Plasticity -- Spike-timing dependent plasticity |
| Session: |
58. Spike Timing II Poster |
| Presentation Time: | Saturday, October 23, 2004 4:00 PM-5:00 PM |
| Location: | San Diego Convention Center - Hall A-H, Board # Q1 |
| Keywords: | LTD, CANNABINOIDS, ACCUMBENS, ADDICTION |
Evidences suggest that both single and repeated exposure to addictive drugs can alter synaptic plasticity in the brain reward pathway. Despite its widespread use, the effects of cannabis derivatives on synaptic transmission and plasticity remain poorly understood. We evaluated the consequences of single and repeated in-vivo exposure to Δ9-Tetrahydrocannabinol (THC), the principal psychoactive ingredient of cannabis, in the nucleus accumbens (NAc), a key structure of the brain reward pathway where we have previously described an endocannabinoid mediated long-term depression (eCB-LTD) induced by sustained cortical activation (10 min @ 13Hz) (Robbe et al., 2002). First, we found that a single exposure of mice to a non-aversive dose of THC (3mg/kg) abolished the retrograde signalling responsible for eCB-LTD one day after in-vivo treatment. This effect was reversed within three days and associated with a marked functional desensitization of cannabinoid CB1 receptors (Mato et al., 2004). Second, we found that after one week of daily in-vivo THC, although CB1R are desensitized, internalized and uncoupled from Gi/o proteins, NAc synapses unexpectedly express normal LTD. This recovery was due to a switch in the mechanisms underlying LTD. Mild stimulation (5 min @ 10Hz) failed to trigger LTD in THC-treated mice, suggesting that the counter adaptation functions as a high pass filter allowing recovery of synaptic plasticity only in response to high cortical activity.
Mato S, Chevaleyre V, Robbe D, Pazos A, Castillo PE, Manzoni OJ (2004) A single
exposure to Delta-9-tetrahydrocannabinol blocks endocannabinoid mediated synaptic
plasticity. Nat Neurosci, in press.
Robbe D, Kopf M, Remaury A, Bockaert J, Manzoni OJ (2002) Endogenous
cannabinoids mediate long-term synaptic depression in the nucleus accumbens.
Proc Natl Acad Sci U S A 99:8384-8388.
Mato S, Chevaleyre V, Robbe D, Pazos A, Castillo PE, Manzoni OJ (2004) A single
exposure to Delta-9-tetrahydrocannabinol blocks endocannabinoid mediated synaptic
plasticity. Nat Neurosci, in press.
Robbe D, Kopf M, Remaury A, Bockaert J, Manzoni OJ (2002) Endogenous
cannabinoids mediate long-term synaptic depression in the nucleus accumbens.
Proc Natl Acad Sci U S A 99:8384-8388.
Supported by INSERM, Fondation pour l echerche Médicale and Région Aquitaine
Sample Citation:
[Authors]. [Abstract Title]. Program No. XXX.XX. 2004 Neuroscience Meeting Planner. San Diego, CA: Society for Neuroscience, 2004. Online.
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