Neuroscience 2005 Abstract
| Presentation Number: | 563.2 |
|---|---|
| Abstract Title: | Forebrain GABAergic neurons are not involved in “classical” pharmacological effects of δ-9-tetrahydrocannabinol. |
| Authors: |
Marsicano, G.*1,2
; Monory, K.1,2
; Massa, F.1,2
; Blaudzun, H.1
; Ekker, M.
; Rubenstein, J.
; Eder, M.1
; Zieglgansberger, W.1
; Lutz, B.1,2
1Dept of Physiol Chem, Johannes Gutenberg Univ., Mainz, Germany 2Germany, Duesbergweg 6, 55099, |
| Primary Theme and Topics |
Cognition and Behavior - Animal Cognition and Behavior -- Emotional learning, memory systems, and modulation of memory |
| Secondary Theme and Topics | Neural Excitability, Synapses, and Glia: Cellular Mechanisms<br />- G-Protein Linked Receptors<br />-- Other |
| Session: |
563. Cannabinoids Poster |
| Presentation Time: | Monday, November 14, 2005 2:00 PM-3:00 PM |
| Location: | Washington Convention Center - Hall A-C, Board # UU80 |
| Keywords: | mouse, CB1 receptor, Cre/LoxP, DSI |
The expression of cannabinoid receptor CB1 in distinct neuronal sub-populations of the central nervous system poses the question which neurons mediate the pharmacological effects of cannabinoids in the brain. To start answering this question, the well-known pharmacological actions of delta-9-tetrahydrocannabinol (THC, the primary psychoactive constituent of marijuana) were tested in conventional CB1 knockout mice and in a number of CB1 conditional knockout mouse lines, lacking the expression of the receptor in different neuronal subpopulations. Mutant and wild-type littermates controls were tested in the so-called behavioural “tetrad” battery of pharmacological effects of THC. Results showed that that GABAergic forebrain interneurons are not required for the manifestation of the typical pharmacological/behavioural symptoms produced by THC treatment: hypolocomotion, hypothermia, catalepsy and increase of nociceptive threshold. In order to control for the physiological functionality of CB1 expression in the conditional mutants used, we tested depolarisation induced suppression of inhibition (DSI) and LTD of inhibitory synapses (I-LTD) in the CA1 region of the hippocampus. Importantly, DSI and I-LTD were normally present in mice expressing CB1 only on GABAergic interneurons, whereas they were abolished in mice lacking CB1 from GABAergic neurons. This indicates that the physiological actions of endocannabinoids on GABAergic transmission are conserved in mice not responsive to THC in the “tetrad” battery of tests. Our results show that “classical” pharmacological actions of THC do not depend on functional expression of CB1 on GABAergic interneurons and pave the way to a novel interpretation of cannabinoid pharmacology.
Sample Citation:
[Authors]. [Abstract Title]. Program No. XXX.XX. 2005 Neuroscience Meeting Planner. Washington, DC: Society for Neuroscience, 2005. Online.
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