Chapter 1 - Importance of chloride homeostasis in the operation of rhythmic motor networks

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Abstract

GABA and glycine are classically called “inhibitory” amino acids, despite the fact that their action can rapidly switch from inhibition to excitation and vice versa. The postsynaptic action depends on the intracellular concentration of chloride ions ([Cl]i), which is regulated by proteins in the plasma membrane: the K+–Cl cotransporter KCC2 and the Na+–K+–Cl cotransporter NKCC1, which extrude and intrude Cl ions, respectively. A high [Cl]i leads to a depolarizing (excitatory) action of GABA and glycine, as observed in mature dorsal root ganglion neurons and in motoneurons both early during development and in several pathological conditions, such as following spinal cord injury. Here, we review some recent data regarding chloride homeostasis in the spinal cord and its contribution to network operation involved in locomotion.

Introduction

Synaptic inhibition mediated by GABA and glycine strongly modulates mammalian neuronal networks from the early life to adulthood. The postsynaptic action of these neurotransmitters on GABAA and glycine receptors depends on the intracellular concentration of chloride ions ([Cl]i) in the target cell. In adult healthy neurons, the activation of GABAA and glycine receptors results in an inward flux of Cl and membrane potential hyperpolarization. Therefore, the inhibitory action of glycine and GABA consists in both shunting incoming excitatory currents and moving the membrane potential away from the action potential threshold. This “classical” hyperpolarizing inhibition is not observed in immature neurons; inhibitory postsynaptic potentials (IPSPs) as well as glycine- and GABA-evoked potentials are instead depolarizing and often excitatory (Gao and Ziskind-Conhaim, 1995, Takahashi, 1984, Wu et al., 1992, Ziskind-Conhaim, 1998), because of a high [Cl]i. The [Cl]i is regulated by transporters in the membrane (Delpire and Mount, 2002). Chloride homeostasis and the regulation of those transporters appear as an important emerging mechanism, by which the strength, as well as the polarity, of postsynaptic inhibition can be controlled, even in adult tissue. This review will center on these issues.

Section snippets

Differential control of chloride homeostasis in primary afferents and motoneurons

The transport of Cl by cation–chloride cotransporters is driven by the concentration gradients of cations (Payne et al., 2003; Fig. 1a). The Na+ gradient generated by the Na+/K+-ATPase fuels the inward-directed Cl pump Na+–K+–Cl cotransporter, NKCC1, which is important in active accumulation of intracellular Cl in immature neurons in several brain areas (Dzhala et al., 2005, Ikeda et al., 2003, Plotkin et al., 1997, Sun and Murali, 1999, Vardi et al., 2000). It is down-regulated with

Contribution of chloride homeostasis to cell excitability

According to the classical view, postsynaptic inhibition induced by the activation of GABAA and glycine receptors consists in two mechanisms: shunting incoming excitatory currents and moving the membrane potential away from the action potential threshold. As already mentioned, this hyperpolarization from rest is not observed in immature spinal neurons (Gao and Ziskind-Conhaim, 1995, Takahashi, 1984, Wu et al., 1992, Ziskind-Conhaim, 1998), thereby raising the question of the effect of

Contribution of chloride dynamics to network activity

Maturation of chloride homeostasis affects network activity. There is a switch in the contribution of chloride-mediated conductances to spontaneous activity from excitation to inhibition during late gestation. A rhythmic spontaneous activity can be recorded in vitro very early (~ E12–E14 in rodents), when many lumbar motoneurons are still migrating and extending their peripheral projections (Hanson and Landmesser, 2003). Electrical transmission plays a significant role in the generation of

Primary afferent depolarizations and antidromic discharges as part of the motor network

It is well established that one form of presynaptic inhibition in the vertebrate spinal cord is associated with primary afferent depolarization (PAD, Alvarez-Leefmans et al., 1998, Rudomin, 1990, Rudomin et al., 1993) and that GABA, through the activation of GABAA receptors, plays a major role in the generation of PAD. Axo–axonic interactions between GABAergic terminals and primary afferents have been demonstrated (see Alvarez, 1998, for review). PADs are reduced by GABAA receptor antagonists (

Dysfunction of chloride homeostasis in pathological conditions

The hyperpolarizing shift of ECl from above to below the resting membrane potential in rodent motoneurons occurs during perinatal development, a time window during which pathways descending from the brainstem arrive in the lumbar enlargement (Brocard et al., 1999, Vinay et al., 2000, Vinay et al., 2002). A complete spinal cord transection was performed on the day of birth to investigate the contribution of descending pathways to the maturation of chloride homeostasis (Jean-Xavier et al., 2006).

Conclusion

To conclude, primary afferent terminal and motoneurons exhibit opposite mechanisms for chloride homeostasis. A high [Cl]i maintained by NKCC1 cotransporters is responsible for PADs. The action potentials that are generated by PADs reaching firing threshold have long been considered as an epiphenomenon or an artifact due to the experimental conditions. The ubiquity of their observation in different motor networks underscores the need to investigate their role further. A low [Cl]i is maintained

Acknowledgments

Our study on the plasticity of inhibitory synaptic transmission in the spinal cord is supported by grants (to L.V.) from the French Agence Nationale pour la Recherche, the French Institut pour la Recherche sur la Moelle épinière et l'Encéphale (to L.V.) and the Christopher and Dana Reeve Foundation (VB1-0502-2 and VB2-0801-2). K.S. received a grant from the Association Française contre les Myopathies (Grant 13912). S.T. received a grant from the Fondation pour la Recherche Médicale (Grant

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