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Cited by 48Neuroscience and Neuropharmacology ResearchNeural dynamics and brain functionReceptor Mechanisms and Signaling

Group II metabotropic glutamate receptors inhibit glutamate release at thalamocortical synapses in the developing somatosensory cortex

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Mateo, Z., Porter, J.T.·2007·Neuroscience
DOI 10.1016/j.neuroscience.2007.02.053PMC PMC3690373
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Abstract

Thalamocortical synapses provide a strong glutamatergic excitation to cortical neurons that is critical for processing sensory information. Unit recordings in vivo indicate that metabotropic glutamate receptors (mGluRs) reduce the effect of thalamocortical input on cortical circuits. However, it is not known whether this reduction is due to a reduction in glutamate release from thalamocortical terminals or from a decrease in cortical neuron excitability. To directly determine whether mGluRs act as autoreceptors on thalamocortical terminals, we examined the effect of mGluR agonists on thalamocortical synapses in slices. Thalamocortical excitatory postsynaptic currents (EPSCs) were recorded in layer IV cortical neurons in developing mouse brain slices. The activation of group II mGluRs with (2S,2'R,3'R)-2-(2',3'-dicarboxycyclopropyl)glycine (DCG IV) reduced thalamocortical EPSCs in both excitatory and inhibitory neurons, while the stimulation of group I or group III mGluRs had no effect on thalamocortical EPSCs. Consistent with a reduction in glutamate release, DCG IV increased the paired pulse ratio and the coefficient of variation of the EPSCs. The reduction induced by DCG IV was reversed by the group II mGluR antagonist, LY341495, and mimicked by another selective group II agonist, (2R,4R)-4-aminopyrrolidine-2,4-dicarboxylic acid (APDC). The mGluR2 subtype appears to mediate the reduction of thalamocortical EPSCs, since the selective mGluR3 agonist, N-acetylaspartylglutamate (NAAG), had no effect on the EPSCs. Consistent with this, we showed that mGluR2 is expressed in the barrels. Furthermore, blocking group II mGluRs with LY341495 reduced the synaptic depression induced by a short stimulus train, indicating that synaptically released glutamate activates these receptors. These results indicate that group II mGluRs modulate thalamocortical processing by inhibiting glutamate release from thalamocortical synapses. This inhibition provides a feedback mechanism for preventing excessive excitation of cortical neurons that could play a role in the plasticity and refinement of thalamocortical connections during this early developmental period.

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  • mGluR2 receptors sit presynaptically on glutamatergic terminals and, when activated by glutamate spillover, reduce glutamate release.

    “Metabotropic GluR2 receptors are located on presynaptic glutamatergic terminals where they are activated by glutamate spillover to inhibit glutamate release (Mateo and Porter 2007).”

    From Short- and Long-Term Consequences of Nicotine Exposure during Adolescence for Prefrontal Cortex Neuronal Network Function (2012) · cites this paper as Mateo and Porter 2007

  • At the thalamocortical synapse, mGluR LTD acts presynaptically to decrease transmitter release and depress synaptic activity, and such a mechanism would be unlikely to result in synapse loss and spine involution and therefore would not be a strong candidate for LTD-facilitated synaptic pruning during adolescence.

    “However, at the thalamocortical synapse, mGluR LTD acts presynaptically to decrease transmitter release and depress synaptic activity.127 Such a mechanism would be unlikely to result in synapse loss and spine involution and therefore would not be a strong candidate for LTD-facilitated synaptic pruning during adolescence.”

    From A role for synaptic plasticity in the adolescent development of executive function (2013) · cites this paper as [127]

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Authors
Mateo, Z., & Porter, J. T.
Affiliations
Ponce Health Sciences University (PR)
Corresponding author
Porter, J.T.
ORCID
Porter, J.T.
Venue
Neuroscience
Publisher
Elsevier BV
Published
2007-05
Volume
146
Issue
3
Pages
1062-1072
ISSN
0306-4522 (ISSN-L)
DOI
10.1016/j.neuroscience.2007.02.053
PMC
PMC3690373
OpenAlex
W2100877613
Cited by
48
References
71
Citations by year
2025: 2 · 2023: 1 · 2022: 2 · 2021: 3 · 2020: 1 · 2019: 3 · 2018: 2 · 2017: 2 · 2016: 2 · 2015: 2 · 2014: 1 · 2013: 7 · 2012: 6
FWCI
1.46
Type
journal article
Language
en
Open access
Licence
Locations
  • Neuroscience (publishedVersion)
  • PubMed (publishedVersion)
  • Europe PMC (PubMed Central) (acceptedVersion)
  • PubMed Central (acceptedVersion)
Funders
National Institutes of Health (F34 GM070406, S06 GM08239)
Topics
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
  • Life Sciences › Neuroscience › Cognitive Neuroscience › Neural dynamics and brain function
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Receptor Mechanisms and Signaling
Keywords
glutamate release, group II metabotropic glutamate receptors, mGluR2, thalamocortical synapses, autoreceptors, DCG-IV, LY341495, pyrrolidine dithiocarbamate, N-acetylaspartylglutamate, excitatory postsynaptic currents, synaptic depression, barrel cortex, cortical excitability
MeSH terms
Amino Acids, Animals, Anticonvulsants, Cerebral Cortex, Cyclopropanes, Electrophysiology, Glycine, Immunohistochemistry, Somatosensory Cortex, Synapses, Thalamus, Xanthenes, Receptors, Presynaptic, Receptors, Metabotropic Glutamate, Excitatory Amino Acid Agonists, Excitatory Amino Acid Antagonists, Glutamic Acid, Excitatory Postsynaptic Potentials, Mice, In Vitro Techniques

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