The metabotropic glutamate receptor (mGluRlα) is concentrated at perisynaptic membrane of neuronal subpopulations as detected by immunogold reaction

Baude, Agnès; Nusser, Zoltán; Roberts, J. D. B.; Mulvihill, Eileen R.; Mcllhinney, R.A. Jeffrey; Somogyi, Péter

doi:10.1016/0896-6273(93)90086-7

Cited by 884 publications

(704 citation statements)

References 69 publications

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“…This observation is of particular interest in view of previous data indicating that the contribution of mGluRs to excitatory responses is significant only after activation by highfrequency stimuli (Bashir et al, 1993;Miles and Poncer, 1993). The evidence for the preferential extrasynaptic localization of mGluRs (Baude et al, 1993) is also indicative for a functional role of these glutamate receptors under conditions of highfrequency stimulation.…”

Section: Discussionmentioning

confidence: 61%

“…5C), corroborates and extends previous observations. Thus, large horizontal O-LM cells (type I) had been shown to express high levels of mGluR1 protein (Baude et al, 1993). In another in situ hybridization study, mGluR1 expression was found in somatostatinpositive (here type I) but not in parvalbumin-positive (here type III) interneurons, whereas mGluR5 expression was detected both in somatostatin-and parvalbumin-positive interneurons (Kerner et al, 1997).…”

Section: Discussionmentioning

confidence: 98%

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Differential Expression of Group I Metabotropic Glutamate Receptors in Functionally Distinct Hippocampal Interneurons

et al. 2000

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Metabotropic glutamate receptors (mGluRs) have been proposed to be involved in oscillatory rhythmic activity in the hippocampus. However, the subtypes of mGluRs involved and their precise distribution in different populations of interneurons is unclear. In this study, we combined functional analysis of mGluR-mediated inward currents in CA1 oriens-alveus interneurons with anatomical and immunocytochemical identification of these interneurons and expression analysis of group I mGluR using single-cell reverse transcription-PCR (RT-PCR). Four major interneuron subtypes could be distinguished based on the mGluR-mediated inward current induced by the application of 100 M trans-(1S,3R)-1-aminocyclopentane-1,3-dicarboxylic acid (ACPD) under voltage-clamp conditions and the action potential firing pattern under current-clamp conditions. Type I interneurons responded with a large inward current of ϳ224 pA, were positive for somatostatin, and the majority expressed both mGluR1 and mGluR5. Type II interneurons responded with an inward current of ϳ80 pA, contained calbindin, and expressed mainly mGluR1. Type III interneurons responded with an inward current of ϳ60 pA. These interneurons were fast-spiking, contained parvalbumin, and expressed mainly mGluR5. Type IV interneurons did not respond with an inward current upon application of ACPD, yet they expressed group I mGluRs. Activation of group I mGluRs under currentclamp conditions increased spike frequency and resulted in rhythmic firing activity in type I and II, but not in type III and IV, interneurons. RT-PCR results suggest that activation of mGluR1 in the subsets of GABAergic interneurons, classified here as type I and II, may play an important role in mediating synchronous activity.

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Section: Discussionmentioning

confidence: 61%

Section: Discussionmentioning

confidence: 98%

Differential Expression of Group I Metabotropic Glutamate Receptors in Functionally Distinct Hippocampal Interneurons

et al. 2000

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“…An important issue to consider is the exact localization of these glutamate receptors in relation to the release sites of glutamate. In contrast to AMPA receptor subunits, which are mainly concentrated in the main body of asymmetric glutamatergic synapses (Petralia et al, 1992;Baude et al, 1995), both mGluR1a and mGluR5 are largely extrasynaptic or perisynaptic to glutamatergic synapses (Baude et al, 1993;Ottersen and Landsend, 1997;Galvan et al, 2006). In light of data showing that increased glutamatergic transmission at cortical synapses may account for the raise in extracellular glutamate measured in the accumbens after acute cocaine administration , the rapid internalization of AMPA receptors following such treatment is predictable because of the increase of glutamate in the synaptic cleft.…”

Section: Discussionmentioning

confidence: 95%

Subcellular and subsynaptic localization of group I metabotropic glutamate receptors in the nucleus accumbens of cocaine-treated rats

2008

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There is significant pharmacological and behavioral evidence that group I metabotropic glutamate receptors (mGluR1a and mGluR5) in the nucleus accumbens play an important role in the neurochemical and pathophysiological mechanisms that underlie addiction to psychostimulants. To further address this issue, we undertook a detailed ultrastructural analysis to characterize changes in the subcellular and subsynaptic localization of mGluR1a and mGluR5 in the core and shell of nucleus accumbens following acute or chronic cocaine administration in rats. After a single cocaine injection (30mg/kg) and 45 minutes withdrawal, there was a significant decrease in the proportion of plasma membrane-bound mGluR1a in accumbens shell dendrites. Similarly, the proportion of plasma membrane-bound mGluR1a was decreased in large dendrites of accumbens core neurons following chronic cocaine exposure (i.e. 1 week treatment followed by three weeks withdrawal). However, neither acute nor chronic cocaine treatments induced significant change in the localization of mGluR5 in accumbens core and shell, which is in contrast with the significant reduction of plasma membranebound mGluR1a and mGluR5 induced by local intra-accumbens administration of the group I mGluR agonist, DHPG. In conclusion, these findings demonstrate that cocaine-induced glutamate imbalance (Smith et al., 1995;Pierce et al., 1996;Reid et al., 1997) has modest effects on the trafficking of group I mGluRs in the nucleus accumbens. These results provide valuable information on the neuroadaptive mechanisms of accumbens group I mGluRs in response to cocaine administration.

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“…mGluR1s inhibit GABAergic transmission at the synapses between molecular layer interneurons and Purkinje cells mGluR1 is the only group I mGluR isoform expressed in cerebellar Purkinje cells (Baude et al, 1993;Negyessy et al, 1997). On Purkinje cell dendrites, these receptors can be located in close apposition not only to glutamatergic terminals but also to GABAergic ones (Baude et al, 1993).…”

Section: Resultsmentioning

confidence: 99%

Group I Metabotropic Glutamate Receptors Inhibit GABA Release at Interneuron-Purkinje Cell Synapses through Endocannabinoid Production

Galante

Diana²

2004

J. Neurosci.

109

100

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Actions of endocannabinoids in the cerebellum can be demonstrated following distinct stimulation protocols in Purkinje cells. First, depolarization-induced elevations of intracellular Ca 2ϩ lead to the suppression of neurotransmitter release from both inhibitory and excitatory afferents. In another case, postsynaptic group I metabotropic glutamate receptors (mGluRs) trigger a strong inhibition of the glutamatergic inputs from parallel and climbing fibers. Both pathways involve endocannabinoids retrogradely acting on type 1 cannabinoid receptors (CB1Rs) at presynaptic terminals. Here, we show that group I mGluR activation also depresses GABAergic transmission at the synapses between molecular layer interneurons and Purkinje cells. Using paired recordings, we found that application of the group I mGluR agonist (RS)-3,5-dihydroxyphenylglycine reduced the evoked IPSCs in Purkinje cells. This effect was independent of postsynaptic Ca 2ϩ increases and was completely blocked by a CB1R antagonist.Experiments performed with the GTP-analogues GDP-␤S and GTP-␥S provided evidence that endocannabinoids released after G-protein activation can also inhibit GABAergic inputs onto nearby, unstimulated Purkinje cells. Block of the enzymes DAG lipase or phospholipase C reduced the group I mGluR-dependent inhibition, suggesting that 2-arachidonyl glycerol could act as retrograde messenger. Finally, group I mGluR activation by brief bursts of activity of the parallel fibers induced a short-lived depression of spontaneous IPSCs via presynaptic CB1Rs. Our results reveal a mechanism with potential physiological importance, by which glutamatergic synapses induce an endocannabinoid-mediated inhibition of the GABAergic inputs onto Purkinje cells.

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The metabotropic glutamate receptor (mGluRlα) is concentrated at perisynaptic membrane of neuronal subpopulations as detected by immunogold reaction

Cited by 884 publications

References 69 publications

Differential Expression of Group I Metabotropic Glutamate Receptors in Functionally Distinct Hippocampal Interneurons

Differential Expression of Group I Metabotropic Glutamate Receptors in Functionally Distinct Hippocampal Interneurons

Subcellular and subsynaptic localization of group I metabotropic glutamate receptors in the nucleus accumbens of cocaine-treated rats

Group I Metabotropic Glutamate Receptors Inhibit GABA Release at Interneuron-Purkinje Cell Synapses through Endocannabinoid Production

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