Acetylcholine Controls GABA-, Glutamate-, and Glycine-Dependent Giant Depolarizing Potentials that Govern Spontaneous Motoneuron Activity at the Onset of Synaptogenesis in the Mouse Embryonic Spinal Cord - CNRS - Centre national de la recherche scientifique Accéder directement au contenu
Article Dans Une Revue Journal of Neuroscience Année : 2014

Acetylcholine Controls GABA-, Glutamate-, and Glycine-Dependent Giant Depolarizing Potentials that Govern Spontaneous Motoneuron Activity at the Onset of Synaptogenesis in the Mouse Embryonic Spinal Cord

Antonny Czarnecki
  • Fonction : Auteur
Herve Le Corronc
  • Fonction : Auteur
Chiara Rigato
  • Fonction : Auteur
Barbara Le Bras
  • Fonction : Auteur
Francois Couraud
  • Fonction : Auteur
Anne-Laure Scain
  • Fonction : Auteur
Anne-Emilie Allain
  • Fonction : Auteur
Christine Mouffle
  • Fonction : Auteur
Erika Bullier
  • Fonction : Auteur
Pascal Branchereau
  • Fonction : Auteur

Résumé

A remarkable feature of early neuronal networks is their endogenous ability to generate spontaneous rhythmic electrical activity independently of any external stimuli. In the mouse embryonic SC, this activity starts at an embryonic age of similar to 12 d and is characterized by bursts of action potentials recurring every 2-3 min. Although these bursts have been extensively studied using extracellular recordings and are known to play an important role in motoneuron (MN) maturation, the mechanisms driving MN activity at the onset of synaptogenesis are still poorly understood. Because only cholinergic antagonists are known to abolish early spontaneous activity, it has long been assumed that spinal cord (SC) activity relies on a core network of MNs synchronized via direct cholinergic collaterals. Using a combination of whole-cell patch-clamp recordings and extracellular recordings in E12.5 isolated mouse SC preparations, we found that spontaneous MN activity is driven by recurrent giant depolarizing potentials. Our analysis reveals that these giant depolarizing potentials are mediated by the activation of GABA, glutamate, and glycine receptors. We did not detect direct nAChR activation evoked by ACh application on MNs, indicating that cholinergic inputs between MNs are not functional at this age. However, we obtained evidence that the cholinergic dependency of early SC activity reflects a presynaptic facilitation of GABA and glutamate synaptic release via nicotinic AChRs. Our study demonstrates that, even in its earliest form, the activity of spinal MNs relies on a refined poly-synaptic network and involves a tight presynaptic cholinergic regulation of both GABAergic and glutamatergic inputs.

Dates et versions

hal-01542731 , version 1 (20-06-2017)

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Citer

Antonny Czarnecki, Herve Le Corronc, Chiara Rigato, Barbara Le Bras, Francois Couraud, et al.. Acetylcholine Controls GABA-, Glutamate-, and Glycine-Dependent Giant Depolarizing Potentials that Govern Spontaneous Motoneuron Activity at the Onset of Synaptogenesis in the Mouse Embryonic Spinal Cord. Journal of Neuroscience, 2014, 34 (18), pp.6389-6404. ⟨10.1523/JNEUROSCI.2664-13.2014⟩. ⟨hal-01542731⟩
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