The function of oligodendrocytes is to ensheath axons with myelin and to both support myelin production and ensure that it myelinates axons in the optimal fashion. Myelin is essential for action potential conduction and acts to increase the speed of action potential firing. Immature axons are premyelinated and separated into groups by primitive sheetlike glial processes from immature undifferentiated glial cells. This gives way to more organized wrapping of the axons with myelin by the oligodendrocytes. The myelin sheet extends from oligodendrocytes and is connected to the cell body via only a very thin process. During the process of myelination, the oligodendro-cyte cell body remains stationary and the myelin sheet wraps around the axon. The myelin sheet is assembled at the local level as it sits close to the axon during the ensheathing process. There are several points to bear in mind about myelination. Oligodendrocytes myelinate more than one axon and can myelinate axons of different diameters. Despite a common cell body, myelin sheaths that myelinate large-diameter axons are thicker than myelin sheaths myelinating small-diameter axons. At the time of myelination it appears that axons secrete molecules at the site of myelination that control the behavior of myelinating oligodendrocytes. The process is not fully understood, but it appears that there is an increase in the intramembra-nous particles (IMPs) on the protoplasmic side of the axon membrane. This occurs during the initiation of myelination and has been hypothesized to be the promoter of myelination.

Multiple sclerosis is a condition that occurs due to demyelination of central axons. The white matter lesions that define this disease are visible by T2-weighted MRI. The condition is due to an autoimmune inflammatory response that results in focal lesions in the CNS. The condition starts with an increase in the permeability of the blood-brain barrier in association with inflammation. The area of abnormality increases over a period of several weeks but then diminishes, leaving a scar that may be gliotic or may exhibit axon degeneration. Function decreases in tandem with the increasing lesion size, but then returns completely as the lesion diminishes. However, over time the attacks recur and function diminishes. Lesion sites have been shown to contain expanded extracellular space due to the loss of axons. This loss of axons results in dysfunction that can lead to limb paralysis and the eventual inability to walk. The potential for treating multiple sclerosis is determined by two main factors: remyelination of axons and replacement of dead axons. The first area is a subject of intense research, with stem cell transplants appearing to offer the best chance of success. Injection of immature oligodendrocytes into rat brain has indicated that they are capable of remyelination, but direction of this process remains a problem. Axon death can be countered by devising neuroprotective strategies for axons during acute attacks. In this it is similar to neuroprotective strategies during ischemic stroke. The advantage in the case of multiple sclerosis is that the attacks when axons die are clinically apparent, and thus therapy could be timed to coincide with attacks.

Breaking Bulimia

Breaking Bulimia

We have all been there: turning to the refrigerator if feeling lonely or bored or indulging in seconds or thirds if strained. But if you suffer from bulimia, the from time to time urge to overeat is more like an obsession.

Get My Free Ebook

Post a comment