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Phasic and Tonic mGlu7 Receptor Activity Modulates the Thalamocortical Network
Valériane Tassin1, Benoît Girard1, Apolline Chotte1
1CNRS, Institut de Génomique Fonctionnelle, UMR-5203Montpellier, France; INSERM, U1191Montpellier, France; UMR-5203, Université de MontpellierMontpellier, France.
Frontiers in Neural Circuits
|May 21, 2016
Summary
Metabotropic glutamate receptor 7 (mGlu7) normally prevents absence seizures by tonically inhibiting thalamic synapses. Blocking mGlu7 activity in vivo triggers seizures, highlighting its crucial physiological role.
Area of Science:
- Neuroscience
- Neuropharmacology
- Epilepsy Research
Background:
- Metabotropic glutamate receptor 7 (mGlu7) mutations are linked to absence-like epileptic seizures.
- The specific function of mGlu7 within the somatosensory thalamocortical network is not well understood.
Purpose of the Study:
- To investigate the role of mGlu7 in modulating neurotransmission at mouse thalamic synapses.
- To explore the in vivo consequences of inhibiting mGlu7 activity.
Main Methods:
- Electrophysiological recordings in mouse thalamic slices.
- Optogenetic and pharmacological manipulation of mGlu7 activity.
- In vivo administration of an mGlu7 negative allosteric modulator (ADX71743).
Main Results:
- mGlu7 is expressed at both glutamatergic and GABAergic thalamic synapses, inhibiting neurotransmission and regulating short-term plasticity.
- mGlu7's inhibitory effects are dependent on its PDZ-ligand.
- Pharmacological inactivation of mGlu7 enhances thalamic synaptic transmission.
- In vivo blockade of mGlu7 induces absence seizure-like behaviors.
Conclusions:
- mGlu7 exerts tonic control over thalamic synaptic transmission, preventing pathological network oscillations.
- mGlu7 plays a critical physiological role in suppressing absence seizures.
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