nervous system 2 myelin
Demyelinating Diseases
1. Multiple sclerosis
Multiple sclerosis
Demyelinating Diseases is the most common Autoimmune disorder in which cells of the immune system fail to recognize the myelin as "self", and begin attacking it. Results in inflammation which causes scarring (sclerosis) around the nerves. Slows or blocks nerve impulses resulting in decreased muscle coordination and strength, and disturbances of sensation and vision.
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In a resting (unstimulated) axon, the inside of the axolemma is negative relative to the outside of the membrane. An impulse or action potential causes a rapid and transient shift in the polarity across the membrane.
Demyelination in the CNS
In progressive multifocal leukoencephalopathy, lesions appear, gradually demyelinating the nerve cells (white matter) of the brain, causing loss of coordination and weakness.
Regeneration of Nervous Tissue: PNS
In the PNS, some repair is possible under certain conditions: The damaged neuron(s) are part of a myelinated nerve, and the neurilemmocytes (Schwann cells) are active and intact. If the cell body (soma) is undamaged
How Does Myelin Increase Rate of Impulse Conduction?
In unmyelinated axons, the impulse must travel continuously the entire length of the axon. The plasma membrane of the axon must depolarize in a continuous wave. Depolarization is a flip-flop of positive and negative charge on the inside and outside of the axon membrane.
Myelination
Most axons are surrounded by an insulating layer of lipid combined with protein called myelin. The myelin sheath functions to electrically insulate the axon. This greatly increases the speed of conduction of nerve impulses. The amount of myelination increases from birth through adulthood.
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Myelination in the CNS and PNS is achieved by different types of neuroglia.
Regeneration of Nervous Tissue
Neurons have a very limited ability to regenerate if injured. Structurally too complex to replicate or repair. Very complex interactions with other neurons. Beginning before birth until about 6 months of age, all developing neurons have lost their ability to undergo mitosis. Once destroyed, they can't be replaced. In the CNS, repair is practically non-existent.
Regeneration of an Injured Axon: conditions, explain
Nissl substance (mRNA & rRNA) is synthesized and protein synthesis increases. Although the axon and its myelin sheath degenerated, the neurilemma remains intact. This is important because without the neurilemma the new regenerating axon could not grow back exactly to the appropriate receptor or effector with which it formed a synapse. Neurilemmocytes on either side of the injury begin to multiply mitotically and form a tube that bridges across the injured area. This tube guides the regenerating axon exactly back to its site of contact with the receptor or effector. Axons grow at a rate of about 1-1.5 mm/day.
CNS: Myelination
Oligodendrocytes send out branches that can myelinate segments of 3-50 axons.
PNS Myelination
Schwann cells or neurilemmocytes myelinate a segment of a single axon. In the PNS, each Schwann cell wraps around about a 1 mm length of an axon and spirals around it many times. Note: the neurilemma is the peripheral, nucleated cytoplasm and is only found in the PNS
Impulse Conduction in a Myelinated Axon:
saltatory Impulse "jumps" from node to node instead of depolarizing the entire length of the axon. This speeds up conduction.
Regeneration of an Injured Axon: list steps
1. Fragmentation of axon and myelin occurs in the distal stump. 2. Wallerian degeneration: degeneration of axon distal to the injury site 3. Cord of Schwann cells follows the path of the original axon. 4. Axon grows into the site of injury, and Schwann cells wrap around it.
Injury to an Axon of the PNS
1. Nucleus migrates to periphery and Nissl bodies break down (=chromatolysis). 2. Axon distal to the site of injury degenerates along with its myelin sheath. - Wallerian degeneration - Macrophages remove cellular debris. 3. A portion of the axon proximal to the injury site degenerates, but only to the first node of Ranvier.