Activation of Group II Metabotropic Glutamate Receptors Inhibits Synaptic Excitation of the Substantia Nigra Pars Reticulata

Bradley, Stefania Risso; Marino, Michael J.; Wittmann, Marion; Rouse, Susan T.; Awad, Hazar; Levey, Allan I.; Conn, P. Jeffrey

doi:10.1523/jneurosci.20-09-03085.2000

Cited by 141Neurological disorders and treatmentsNeuroscience and Neuropharmacology ResearchParkinson's Disease Mechanisms and Treatments

Activation of Group II Metabotropic Glutamate Receptors Inhibits Synaptic Excitation of the Substantia Nigra Pars Reticulata

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Bradley, Stefania Risso, Marino, Michael J., Wittmann, Marion, Rouse, Susan T., Awad, Hazar, Levey, Allan I., Conn, P. Jeffrey·2000·The Journal of Neuroscience

DOI 10.1523/jneurosci.20-09-03085.2000PMC PMC6773118

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Abstract

Loss of nigrostriatal dopaminergic neurons in Parkinson's disease (PD) leads to increased activity of glutamatergic neurons in the subthalamic nucleus (STN). Recent studies reveal that the resultant increase in STN-induced excitation of basal ganglia output nuclei is responsible for the disabling motor impairment characteristic of PD. On the basis of this, it is possible that any manipulation that reduces activity at excitatory STN synapses onto basal ganglia output nuclei could be useful in the treatment of PD. We now report that group II metabotropic glutamate receptors (mGluRs) are presynaptically localized on STN terminals and that activation of these receptors inhibits excitatory transmission at STN synapses. In agreement with the hypothesis that this could provide a therapeutic benefit in PD, a selective agonist of group II mGluRs induces a dramatic reversal of catalepsy in a rat model of PD. These results raise the exciting possibility that selective agonists of group II mGluRs could provide an entirely new approach to the treatment of PD. These novel therapeutic agents would provide a noninvasive pharmacological treatment that does not involve the manipulation of dopaminergic systems, thus avoiding the problems associated with current therapies.

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Activation of mGluR2s can inhibit GABA release through a presynaptic mechanism.
“It was shown that activation of mGluR2s can also regulate release of other neurotransmitters: it can inhibit GABA release via a presynaptic mechanism (Bradley et al. 2000; Pilc et al. 2008).”
From Short- and Long-Term Consequences of Nicotine Exposure during Adolescence for Prefrontal Cortex Neuronal Network Function (2012) · cites this paper as Bradley et al. 2000
In the section on the presynaptic mechanism (page unavailable), the paper says group II mGluRs likely inhibit glutamate release from presynaptic terminals, not GABA release. Its reference to GABAergic neurons identifies the cells receiving that excitatory input; it does not identify the transmitter being released by the affected terminals. (LLM, conf=0.88)
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Activation of groups I or III metabotropic glutamate receptors inhibits excitatory transmission in the rat subthalamic nucleus
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Dopamine Modulates the Function of Group II and Group III Metabotropic Glutamate Receptors in the Substantia Nigra Pars Reticulata
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Activation of group II metabotropic glutamate receptors induces long-term depression of excitatory synaptic transmission in the substantia nigra pars reticulata
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Activation of Group I Metabotropic Glutamate Receptors Produces a Direct Excitation and Disinhibition of GABAergic Projection Neurons in the Substantia Nigra Pars Reticulata
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Metabotropic Glutamate Receptor mGluR4 as a Novel Target for Parkinson's Disease
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Authors: Bradley, S. R., Marino, M. J., Wittmann, M., Rouse, S. T., Awad, H., Levey, A. I., & Conn, P. J.
Affiliations: University of Tübingen (DE)
Emory University (US)
ORCID: Marino, Michael J.
Levey, Allan I.
Conn, P. Jeffrey
Venue: The Journal of Neuroscience
Publisher: Society for Neuroscience
Published: 2000-05-01
Volume: 20
Issue: 9
Pages: 3085-3094
ISSN: 0270-6474 (ISSN-L)
1529-2401
DOI: 10.1523/jneurosci.20-09-03085.2000
PMC: PMC6773118
OpenAlex: W1926939570
Cited by: 141
References: 54
Citations by year: 2026: 1 · 2025: 2 · 2024: 1 · 2023: 1 · 2022: 2 · 2021: 2 · 2020: 5 · 2019: 1 · 2018: 4 · 2017: 4 · 2016: 2 · 2015: 4 · 2014: 5 · 2013: 5 · 2012: 6
FWCI: 10.28
Type: journal article
Language: en
Open access: hybrid
doi.org
Licence: cc-by-nc-sa
creativecommons.org/licenses/by-nc-sa/4.0/ (vor, 184 d)
Locations: Journal of Neuroscience (publishedVersion, cc-by-nc-sa)
PubMed Central (publishedVersion)
PubMed (publishedVersion)
Journal of Neuroscience Nursing
Funders: National Parkinson Foundation
Emory University
National Institutes of Health
U.S. Army
Parkinsonfonden
Topics: Health Sciences › Medicine › Neurology › Neurological disorders and treatments
Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
Health Sciences › Medicine › Neurology › Parkinson's Disease Mechanisms and Treatments
Keywords: group II metabotropic glutamate receptors, substantia nigra pars reticulata, subthalamic nucleus, Parkinson's disease, basal ganglia, glutamatergic synapses, presynaptic inhibition, catalepsy, mGluR agonists, glutamatergic neurons
MeSH terms: Animals, Bridged Bicyclo Compounds, Catalepsy, Haloperidol, Male, Parkinson Disease, Substantia Nigra, Rats, Sprague-Dawley, Receptors, Presynaptic, Receptors, Metabotropic Glutamate, Dopamine Antagonists, Excitatory Amino Acid Agonists, Glutamic Acid, Excitatory Postsynaptic Potentials, Subthalamic Nucleus, Rats

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Activation of Group II Metabotropic Glutamate Receptors Inhibits Synaptic Excitation of the Substantia Nigra Pars Reticulata

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