Potassium spatial buffering is a mechanism for the regulation of extracellular potassium concentration by astrocytes. Other mechanisms for astrocytic potassium clearance are carrier-operated, or channel-operated potassium-chloride uptake. The repolarization of neurons tends to increase potassium concentration in the extracellular matrix. If a significant rise occurs, it will reduce the concentration gradient across the neuronal membrane, resulting in depolarization. This resulting depolarization will lead to increased excitability or spontaneous firing. Astrocytes have large numbers of potassium ion channels facilitating the removal of potassium ions from the extracellular matrix. They are taken up at one region of the astrocyte and then distributed throughout the cytoplasm of the cell, and to other cells via astrocytic gap junctions. This keeps the level of extracellular potassium contents around a constant value to prevent interference with the normal propagation of an action potential throughout neural transmission.
Potassium Spatial Buffering Glial cells, once believed to have a passive role in CNS, are active regulators of numerous functions in the brain, including clearance of the neurotransmitter from the synapses, guidance during neuronal migration, control of neuronal synaptic transmission, and maintaining an ideal ionic environment for active communications between neurons in central nervous system. Neurons are surrounded by extracellular fluid rich in sodium ions and poor in potassium ions. The concentrations of these ions are reversed inside the cells. Due to the difference in concentration, there is a chemical gradient across the cell membrane, which leads to sodium influx and potassium efflux. When the action potential takes place, a considerable change in extracellular potassium concentration occurs due to the limited volume of the CNS extracellular space. The change in potassium concentration in the extracellular space impacts a variety of neuronal processes, such as maintenance of membrane potential, activation and inactivation of voltage gated channels, synaptic transmission, and electrogenic transport of neurotransmitters. Change of extracellular potassium concentration of from 3mM can affect neural activity. Therefore, there are diverse cellular mechanisms for tight control of potassium ions, the most widely accepted mechanism being K+ spatial buffering mechanism. Orkand and his colleagues who first theorized spatial buffering stated "if a Glial cell becomes depolarized by K+ that has accumulated in the clefts, the resulting current carries K+ inward in the high [K+] region and out again, through electrically coupled Glial cells in low [K+] regions" In the model presented by Orkand and his colleagues, glial cells intake and traverse potassium ions from region of high concentrations to region of low concentration maintaining potassium concentration to be low in extracellular space. Glial cells are well suited for transportation of potassium ions since it has unusually high permeability to potassium ions and traverse long distance by its elongated shape or by being coupled to one another.
Potassium Regulatory Mechanisms Potassium regulation can be broadly categorized into two categories: Potassium uptake and Potassium spatial buffering. Potassium uptake involves the net clearance of excess extracellular potassium ions into astrocytes via the use of transporters like sodium-potassium ATPase or via potassium ion channels. The sodium-potassium pump in astrocytes is required to maintain low extracellular potassium ion levels around neurons. With this, the influx of potassium ions into glial cells is accompanied by the influx of chlorine or the efflux of sodium. Potassium uptake is a distinct mechanism when compared to potassium spatial buffering, in potassium uptake does not involve the redistribution of potassium ions from high to low concentrations via astrocytes. This process particularlay involves removing, or uptaking, high extracellular levels of potassium ions. Potassium spatial buffering depends on functionally coupled astrocytes/glial cells that have high potassium permeability to transfer potassium ions from regions of elevated potassium concentration to regions of lower potassium concentration. This process is often done via glial cell fluxes, which are primarily mediated by inwardly-rectifying potassium ion channels. Potassium current is driven by the difference in glial membrane potential and local potassium equilibrium potential. When one region of potassium concentration increases, there is a net driving force causing potassium to flow into the glial cells. The entry of potassium causes a local depolarization that propagates electrotonically, or via the passive spread of electrical current through the glial cell network. This causes a net efflux of potassium ions out of glial cells, resulting in dispersion of local potassium; thus preventing swelling. These two mechanisms are important for proper neuronal function due to the homeostatic processes distinctly provided by each mechanism to regulate neuronal excitability. Meaning, that neural excitability relies on the precise inward and outward flux of ions that are crucial for carrying out action potentials. The proper maintenance of potassium ion homeostasis is crucial to prevent neuronal hyperexcitability, or the overexcitability of a neuron to fire an action potential.
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