Neuroscience 2002 Abstract
| Presentation Number: | 737.1 |
|---|---|
| Abstract Title: | ACTIVATION OF MUSCARINIC ACETYLCHOLINE RECEPTORS ENHANCES THE RELEASE OF ENDOCANNABINOIDS IN THE HIPPOCAMPUS. |
| Authors: |
Kim, J.*1
; Alger, B. E.1,2
1Program in Neuroscience, University of Maryland, Baltimore, MD 2Department of Physiology, University of Maryland, Baltimore, MD |
| Primary Theme and Topics |
Synaptic Transmission and Excitability - Neurotransmitters -- Cannabinoids |
| Secondary Theme and Topics | Synaptic Transmission and Excitability<br />- G-Protein Linked Receptors<br />-- Muscarinic receptors |
| Session: |
737. Neurotransmitters: cannabinoids I Poster |
| Presentation Time: | Wednesday, November 6, 2002 1:00 PM-2:00 PM |
| Location: | Hall A2-B3 C-48 |
| Keywords: | RETROGRADE, SYNAPTIC TRANSMISSION, LIPID, G PROTEIN |
Endocannabinoids are endogenous compounds that resemble the active ingredient of marijuana and activate the cannabinoid receptor in the brain. They mediate retrograde signaling from principal cells to interneurons. Endocannabinoid is released from pyramidal cells by Ca2+ influx and suppresses GABAergic transmission (depolarization-induced suppression of inhibition, DSI). Activation of group I metabotropic glutamate receptor stimulates the endocannabinoid release. We predicted that additional neurotransmitters would regulate endocannabinoid release. Inhibitory synapses in CA1 region of acute hippocampal slices from rats were studied using whole-cell patch clamp techniques. We found that low dose (0.2 - 0.5 µM) of carbachol enhanced DSI by activating muscarinic acetylcholine receptors (mAChRs) on postsynaptic cells without affecting basal eIPSC amplitude. Higher dose of carbachol (≧ 1 µM) both enhanced DSI and tonically depressed eIPSCs by releasing endocannabinoids. With AM251, a CB1 receptor antagonist, or in CB1-/- mice, carbachol did not produce DSI at 1 - 25 µM, or did not affect basal eIPSC at 1 µM. DSI enhancement by endocannabinoid required an increase in intracellular Ca2+, whereas tonic release of endocannabinoid did not. Muscarinic and glutamatergic regulations of cannabinoid release were independent at receptor level, but shared intracellular machinery. We conclude that activation of mAChR reduces GABA release by enhancing endocannabinoid release. This study shows a new role of the muscarinic cholinergic system in mammalian brain.
Supported by PHS grants RO1 DA14725, RO1 NS30219 (BEA); Training Program in Neuroscience T32 DE1474 (JK)
Sample Citation:
[Authors]. [Abstract Title]. Program No. XXX.XX. 2002 Neuroscience Meeting Planner. Orlando, FL: Society for Neuroscience, 2002. Online.
Copyright © 2002-2025 Society for Neuroscience; all rights reserved. Permission to republish any abstract or part of any abstract in any form must be obtained in writing by SfN office prior to publication.
