Abstract
Maturation of GABA/Glycine chloride-mediated synaptic inhibitions is crucial for the establishment of a balance between excitation and inhibition. GABA and glycine are excitatory neurotransmitters on immature neurons that exhibit elevated [Cl-]i. Later in development [Cl-]i drops leading to the occurrence of inhibitory synaptic activity. This ontogenic change is closely correlated to a differential expression of two cation-chloride cotransporters that are the Cl- channel K+/Cl- co-transporter type 2 (KCC2) that extrudes Cl- ions and the Na+-K+-2Cl- cotransporter NKCC1 that accumulates Cl- ions. The classical scheme built from studies performed on cortical and hippocampal networks proposes that immature neurons display high [Cl-]i because NKCC1 is overexpressed compared to KCC2 and that the co-transporters ratio reverses in mature neurons, lowering [Cl-]i. In this chapter, we will see that this classical scheme is not true in motoneurons (MNs) and that an early alteration of the chloride homeostasis may be involved in pathological conditions.
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