Neuroscience 2004 Abstract
| Presentation Number: | 623.15 |
|---|---|
| Abstract Title: | Metabotropic glutamate receptor subtypes differentially contribute to endocannabinoid release in the hippocampus. |
| Authors: |
Edwards, D. A.*1
; Karnup, S. V.1
; Alger, B. E.1
1Dept. of Physiology, Univ. of Maryland Sch. of Med., Baltimore, MD |
| Primary Theme and Topics |
Synaptic Transmission and Excitability - Neurotransmitters -- Cannabinoids |
| Secondary Theme and Topics | Synaptic Transmission and Excitability<br />- Synaptic Transmission<br />-- Postsynaptic mechanisms: Inhibitory |
| Session: |
623. Cannabinoids II Poster |
| Presentation Time: | Tuesday, October 26, 2004 10:00 AM-11:00 AM |
| Location: | San Diego Convention Center - Hall A-H, Board # J11 |
| Keywords: | DSI, mGluR, inhibition, hippocampus |
The psychoactive component of marijuana, Δ-9-tetrahydrocannabinol, is analogous to the brain’s own endogenous lipids called endocannabinoids. Endocannabinoids are retrograde messengers at inhibitory synapses of the CA1 region of the hippocampus. By modulating GABA release at these synapses, endocannabinoids likely play a significant role in the primary functions of the hippocampus, namely in learning and memory. Endocannabinoids can be released in a Ca2+-dependent or -independent manner and bind to the endocannabinoid receptor, CB1, on presynaptic terminals and suppress the release of GABA. This is seen as a reduction of inhibitory postsynaptic current (IPSC) on the pyramidal cell. Ca2+-dependent endocannabinoid release causes “depolarization induced suppression of inhibition,” (DSI). Activation of the Group I metabotropic receptors (mGluR), which include the two subtypes mGluR1 and mGluR5, on pyramidal cells suppresses IPSC amplitude and enhances DSI. It is not clear what contribution each receptor makes to both the Ca2+-dependent and -independent mechanisms of endocannabinoid release. To clarify the roles of these receptors we studied DSI and suppression of baseline IPSC amplitude in acute hippocampal slices of mGluR1 and mGluR5 knockout mice, using a whole-cell patch clamp technique. We found that activation of mGluR5 decreased IPSC amplitude and enhanced DSI; however, in the mGluR5 knockout mouse, activation of mGluR1 had no effect on baseline IPSC amplitude or DSI. These results show that mGluR5 is responsible for endocannabinoid release through Ca2+-dependent and -independent mechanisms in the mouse, and that mGluR1 is not involved. The conditions and intracellular mechanisms by which a single receptor, mGluR5, can trigger two different pathways should be investigated further.
Supported by NIH NS30219 and DE14625.
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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