About this Research Topic
Changes in the intracellular ion concentration are critically involved in numerous chronic and acute neurological disorders including epilepsies, neuropathic pain, traumatic brain injury (TBI) and cerebrovascular accidents (CVA). One of the first sign of the modified ion homeostasis during pathology is decreased inhibitory strength of GABA and glycine neurotransmission that provokes neuronal spiking, causes epileptic network activity and leads to brain swelling. Although presently the implication of hyperpolarizing to depolarizing shift of GABA and glycine neurotransmission to diverse brain pathologies is well established, the molecular and cellular mechanisms involved in these process are far from being understood.
The inhibitory strength of GABA and glycine neurotransmission depends primarily on the gradients of Cl- and HCO3- anions. The control of both Cl- and HCO3- ion gradients in neurons and glia is achieved by the coordinated action of large number of ion channels, transporters, exchangers and is tightly dependent on the intracellular and extracellular concentrations of Ca, K, Na, and H ions. While recent studies provided important insights on the functioning and pathophysiological roles of transporters related to chloride homeostasis, such as the potassium/chloride co-transporter KCC2 and sodium-potassium/chloride co-transporter NKCC1, the contribution of other players, and particularly the role of H+/HCO3- ion homeostasis, remain obscure. In general the mechanisms regulating ion transporters activity during both physiological and pathological conditions are also poorly understood.
Moreover, the secondary and tertiary structure of the transporters, organization and mechanism controlling the intrinsic transporter activity are open questions.
In this research topic, our emphasis is on outlining progress made in the understanding of the molecular and cellular processes contributing to the control of ionic homeostasis in the brain during different neurological disorders and under physiological conditions. We welcome investigators to contribute through original research articles, perspectives, as well as review articles or case reports that will stimulate the continuing efforts to understand the mechanism underlying this subject.
The inhibitory strength of GABA and glycine neurotransmission depends primarily on the gradients of Cl- and HCO3- anions. The control of both Cl- and HCO3- ion gradients in neurons and glia is achieved by the coordinated action of large number of ion channels, transporters, exchangers and is tightly dependent on the intracellular and extracellular concentrations of Ca, K, Na, and H ions. While recent studies provided important insights on the functioning and pathophysiological roles of transporters related to chloride homeostasis, such as the potassium/chloride co-transporter KCC2 and sodium-potassium/chloride co-transporter NKCC1, the contribution of other players, and particularly the role of H+/HCO3- ion homeostasis, remain obscure. In general the mechanisms regulating ion transporters activity during both physiological and pathological conditions are also poorly understood.
Moreover, the secondary and tertiary structure of the transporters, organization and mechanism controlling the intrinsic transporter activity are open questions.
In this research topic, our emphasis is on outlining progress made in the understanding of the molecular and cellular processes contributing to the control of ionic homeostasis in the brain during different neurological disorders and under physiological conditions. We welcome investigators to contribute through original research articles, perspectives, as well as review articles or case reports that will stimulate the continuing efforts to understand the mechanism underlying this subject.
Important Note: All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.
