Glial Cell

Glial cells are also known as neuroglia, meaning nerve "glue".

Macroglia

 * 1) Astrocytes: they have light cytoplasm, astrocytic filamentous bodies, numerous processes and they can form a glial "scar". Their functions are:
 * 2) to contribute to the extracellular potassium concentration maintenance
 * 3) to cover the basal lamina of the capillaries (part of the blood-brain-barrier) and transport some of the nutrients to neurons through their cytoplasm
 * 4) to cover the surface layer of the CNS (glia limitans)
 * 5) to cover the surface of neurons, fill in the interneuronal spaces
 * 6) by finger-like processes surround and isolate synaptic clefts, astrocytes may contribute to the inactivation of neurotransmitters (GABA, glutamate, glycine)
 * 7) after the brain is damaged, they form astrocytic scar (preventing the regrowth of central axons)
 * 8) Oligodendrocytes: they contribute to the surface cover (myelination) of neuronal bodies and processes (glial cell processes surround unmyelinated fibers, layers of myelin). Oligodendrocyte‘s plasma membrane contains voltage-gated ion channels. Myelin-forming cell furnishes channels for the axon → myelin provides a signal to prevent the insertion of sodium channels into the internodal region of a myelinated nerve fibre.

Microglia
Microglia are functionally similar to macrophages; is probably of mesodermal origin; microglial cells are activated by some pathologic and reparatory processes in the CNS (gliosis)

Ependymal cells
They line the internal cavities of the CNS - part of the blood-brain barrier and they can absorb and secrete cerebrospinal fluid.

Control of extracellular potassium concentration
Glial cells have a resting potential of about -90 mV (more negative than a typical neuronal membrane), which is nearly identical to EK (equilibrium potential for K+). Plasma membrane contains various densities of K+ channels, which are employed in the control of ECF’s [K+], voltage-gated Na+, K+, Ca2+ channels, which incorporated into the neuronal membrane and/or may serve to generation of electrical signals with Ca2+ probably serving as a second messenger. Gap junctions among glia cells provide a low-resistance pathway for intercellular ionic current and a flow of some substances.

During the repolarization phase and the afterhyperpolarization of each neuronal action potential, a small amount of potassium leaves the neurons into the ECF. Following a sustained neuronal activity, a local increase in [K+] can be detected. This increase must be cleared to prevent depolarization of neurons and synaptic terminals in the vicinity, through the following ways:
 * 1) Diffusion (a comparatively slow process)
 * 2) Flow of potassium current through glia (spatial buffering) - as the glial resting potential lies close to EK, increase of extracellular [K+] depolarizes the glial membrane:
 * 3) Since the depolarized cells are somewhat negative to the local EK, potassium enters the cell and serve as charge carriers to the less depolarized regions of the glial syncytium
 * 4) the electrical circuit is completed by the extracellular flow of sodium and chloride ions →
 * 5) redistribution of K+ during the neuronal activity
 * 6) Active transport of extracellular K+ back into neurons back the glia.

Glial cells at the site of an old brain injury are not as efficient in the spacial buffering of potassium ions → tendency for epileptic seizures in regions of an astrocytic scar, due to rise of ECF [K+] → depolarization → increased excitability (e.g.: seizures)