The oligodendrocyte lineage is the sequence of cells that originated from a common initiator cell. Illustrates the development and differentiation from oligodendrocyte precursor cells to fully mature myelin-producing oligodendrocytes[1]. Oligodendrocytes are initially "anterior neuroectodermal cells of the subventricular zones"[1] found in the brain, and subsequently migrate and develop. Pre-GD3 are the initial OPCs that are “monopolar”[1] and develop into motile GD3+ cells, also called O-2A cells, which exist as “bipotential” cells[1] as they have the ability to “differentiate” [1] in an astrocytes or oligodendrocytes in vitro[1]. The path chosen depends on the environment in which it resides[1]. O-2A cells are also called O-2A progenitors[1]. However, in an “in vivo” environment[1], it is not conclusive whether O-2A cells have bipotentiality as in “in vitro”[1]. O-2A cells then evolve into pro-oligodendroblast cells which are then “differentiated”[1] into pre-GalC cells as shown in Figure 1. All of these cells have the ability to increase via proliferation[1]. The next step in the oligodendrocyte lineage is development into immature oligodendrocytes. Once a period of 24-28 hours has elapsed, immature oligodendrocytes develop into mature oligodendrocytes which then have the ability to myelinate[1]. The oligodendrocyte lineage is controlled in many ways. Early developing OPCs tend to be able to proliferate, however in later stages they have a habit of stopping replication and starting to “differentiate” irreversibly[2]. Oligodendrocyte differentiation is controlled via a series of proteins such as “PDGF [platelet-derived growth factor], bFGF, insulin-like growth factor… middle of paper… difference so that the potential for membrane can return to the resting membrane potential of -65mV. This period of repolarization is known as the absolute refractory period since "no new action potentials can be fired"[6] due to the inactivation of voltage-gated sodium ion channels. There comes a point where too many potassium ions leave the nerve cell during repolarization, which becomes hyperpolarized – the membrane potential becomes “even more negative”[5], below -65mV. During hyperpolarization, an action potential can be created since the sodium ion channels are now in their resting state and not all potassium channels are closed yet; however the stimulus must be greater than usual. This is known as the relative refractory period. Voltage-gated sodium ion channels open to allow some sodium ions to flow into the axon to raise the membrane potential up to -65 mV.