Neuroscience 2001 Abstract
| Presentation Number: | 913.16 |
|---|---|
| Abstract Title: | Activation of mGlu4/8 receptors suppresses glutamate release from thalamocortical terminals induced by activation of 5-HT-2A receptors. |
| Authors: |
Zhang, C.*1
; Marek, G. J.1
1Dept Psychiatry, Yale School of Medicine, New Haven, CT |
| Primary Theme and Topics |
Synaptic Transmission and Excitability - G-Protein Linked Receptors -- Metabotropic glutamate receptors |
| Secondary Theme and Topics | Synaptic Transmission and Excitability<br />- Neurotransmitters<br />-- Glutamate |
| Session: |
913. G-protein linked receptors: metabotropic glutamate receptors--physiology and behavior Poster |
| Presentation Time: | Thursday, November 15, 2001 11:00 AM-12:00 PM |
| Location: | Exhibit Hall E-23 |
| Keywords: | metabotropic glutamate, prefrontal cortex, group III mGluR, transmitter release |
Activation of 5-HT2A receptors in the rat prefrontal cortex results in glutamate release (5-HT-induced EPSCs) from thalamocortical afferents (Aghajanian & Marek, 1997 Marek et al., 2001). Activation of both metabotropic glutamate2 receptors (mGluR2) (Marek et al., 2000) and group III mGluR (Lee, Y. et al., 2000, SFN abstr.) suppresses glutamate release from these terminals. The purpose of this study is to investigate whether mGluR4 and/or mGluR8 (group III mGluR) modulate excitatory neurotransmission from these cortical terminals. The group III mGlu antagonist MAP4 suppressed 5-HT-induced EPSCs with an EC50 = 46 µM and maximal suppression of only 29% at 300 µM. MAP4 (300 µM) nearly completely blocked the suppressant action of L-AP4 on 5-HT-induced EPSCs, consistent with a report that MAP4 is a partial agonist at the hmGluR4 (Knopfel et al., 1995). The moderately selective mGluR8 agonist PPG suppressed 5-HT-induced EPSCs with IC50 of ~ 0.4 µM (maximal suppression 93%), though with a shallow slope. The mGlu antagonist LY341495 blocked the suppressant action of PPG (5 µM) on 5-HT-induced EPSCs with an IC50 of 38 µM, which is near the affinity of this mGlu antagonist for the mGluR4 (Kingston et al., 1998). However, an antagonist with a reported 25-fold selectivity for mGluR8 vs. mGluR4 receptors, CPPG (10µM) (Naples & Hampson, 2001) blocked the suppressant action of PPG (5µM) on 5-HT-induced EPSCs: pA2 = 5.85 (1.4 µM). These results suggest that activation of mGluR4 and perhaps mGluR8 may mediate the suppressant action of group III mGlu agonists on 5-HT-induced EPSCs in this unique population of thalamocortical terminals.
Supported by NIMH & NARSAD (GJM)
Sample Citation:
[Authors]. [Abstract Title]. Program No. XXX.XX. 2001 Neuroscience Meeting Planner. San Diego, CA: Society for Neuroscience, 2001. Online.
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