Unipolar neurons have only one structure that extends away from the soma. These neurons are not found in vertebrates but are found in insects where they stimulate muscles or glands. A bipolar neuron has one axon and one dendrite extending from the soma. An example of a bipolar neuron is a retinal bipolar cell, which receives signals from photoreceptor cells that are sensitive to light and transmits these signals to ganglion cells that carry the signal to the brain.
Multipolar neurons are the most common type of neuron. Each multipolar neuron contains one axon and multiple dendrites. Multipolar neurons can be found in the central nervous system brain and spinal cord. An example of a multipolar neuron is a Purkinje cell in the cerebellum, which has many branching dendrites but only one axon.
Pseudounipolar cells share characteristics with both unipolar and bipolar cells. A pseudounipolar cell has a single process that extends from the soma, like a unipolar cell, but this process later branches into two distinct structures, like a bipolar cell.
Most sensory neurons are pseudounipolar and have an axon that branches into two extensions: one connected to dendrites that receive sensory information and another that transmits this information to the spinal cord.
At one time, scientists believed that people were born with all the neurons they would ever have. Research performed during the last few decades indicates that neurogenesis, the birth of new neurons, continues into adulthood.
Neurogenesis was first discovered in songbirds that produce new neurons while learning songs. For mammals, new neurons also play an important role in learning: about new neurons develop in the hippocampus a brain structure involved in learning and memory each day. While most of the new neurons will die, researchers found that an increase in the number of surviving new neurons in the hippocampus correlated with how well rats learned a new task.
Interestingly, both exercise and some antidepressant medications also promote neurogenesis in the hippocampus. Stress has the opposite effect. How do scientists identify new neurons? A researcher can inject a compound called bromodeoxyuridine BrdU into the brain of an animal. A technique called immunohistochemistry can be used to attach a fluorescent label to the incorporated BrdU, and a researcher can use fluorescent microscopy to visualize the presence of BrdU, and thus new neurons, in brain tissue.
This site contains more information about neurogenesis, including an interactive laboratory simulation and a video that explains how BrdU labels new cells. While glia are often thought of as the supporting cast of the nervous system, the number of glial cells in the brain actually outnumbers the number of neurons by a factor of ten. Neurons would be unable to function without the vital roles that are fulfilled by these glial cells. Glia guide developing neurons to their destinations, buffer ions and chemicals that would otherwise harm neurons, and provide myelin sheaths around axons.
Scientists have recently discovered that they also play a role in responding to nerve activity and modulating communication between nerve cells. When glia do not function properly, the result can be disastrous—most brain tumors are caused by mutations in glia. There are several different types of glia with different functions, two of which are shown in Figure Astrocytes , shown in Figure They provide nutrients and other substances to neurons, regulate the concentrations of ions and chemicals in the extracellular fluid, and provide structural support for synapses.
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Proceedings of the National Academy of Sciences. Characterization of cloned cDNA representing rat myelin basic protein: absence of expression in brain of shiverer mutant mice.
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In: Minkowski A, Regional development of the brain in early life. Blackwell, Oxford, 3—70 Also In Anatomy. At the nodes, the axon is exposed to the extracellular space. How is the spiral wrapping of the myelin sheath around axons formed precisely and appropriately?
One mechanism has been identified in PNS myelination. Unmyelinated autonomic neurons express low levels of neuregulin 1 type III on the axon surface, whereas heavily myelinated axons express high levels. Without neuregulin 1 type III, Schwann cells in culture derived from these mutant mice cannot myelinate neurons in the spinal cord dorsal root ganglion neurons.
Intriguingly, in normally unmyelinated fibers, forced expression of neuregulin 1 type III in the postganglionic fibers of sympathetic neurons grown in culture can be forced to myelinate. Furthermore, above the threshold, the myelin formation is correlated with the amount of neuregulin 1 type III presented by the axon to the Schwann cell.
Reduced expression of neuregulin 1 type III leads to a thinner than normal myelin sheath in the heterozygous mutant mice of this molecule. In contrast, transgenic mice that overexpress neuregulin 1 become hypermyelinated. Although several reports show that oligodendrocytes respond to neuregulin 1 in vitro, analyses of a series of conditional null mutant animals lacking neuregulin 1 showed normal myelination Brinkmann et al.
It is still unclear how myelination is regulated in the CNS. How does myelin enhance the speed of action potential propagation? It insulates the axon and assembles specialized molecular structure at the nodes of Ranvier. In unmyelinated axons, the action potential travels continuously along the axons.
For example, in unmyelinated C fibers that conduct pain or temperature 0. In contrast, among the myelinated nerve fibers, axons are mostly covered by myelin sheaths, and transmembrane currents can only occur at the nodes of Ranvier where the axonal membrane is exposed. At nodes, voltage-gated sodium channels are highly accumulated and are responsible for the generation of action potentials. The myelin helps assemble this nodal molecular organization.
For example, during the development of PNS myelinated nerve fibers, a molecule called gliomedin is secreted from myelinating Schwann cells then incorporated into the extracellular matrix surrounding nodes, where it promotes assembly of nodal axonal molecules. Due to the presence of the insulating myelin sheath at internodes and voltage-gated sodium channels at nodes, the action potential in myelinated nerve fibers jumps from one node to the next.
This mode of travel by the action potential is called "saltatory conduction" and allows for rapid impulse propagation Figure 1A. Following demyelination, a demyelinated axon has two possible fates.
The normal response to demyelination, at least in most experimental models, is spontaneous remyelination involving the generation of new oligodendrocytes. In some circumstances, remyelination fails, leaving the axons and even the entire neuron vulnerable to degeneration.
Remyelination in the CNS: from biology to therapy. Nature Reviews Neuroscience 9, — All rights reserved. Figure Detail What happens if myelin is damaged? The importance of myelin is underscored by the presence of various diseases in which the primary problem is defective myelination. Demyelination is the condition in which preexisting myelin sheaths are damaged and subsequently lost, and it is one of the leading causes of neurological disease Figure 2.
Primary demyelination can be induced by several mechanisms, including inflammatory or metabolic causes. Myelin defects also occur by genetic abnormalities that affect glial cells. Regardless of its cause, myelin loss causes remarkable nerve dysfunction because nerve conduction can be slowed or blocked, resulting in the damaged information networks between the brain and the body or within the brain itself Figure 3. Following demyelination, the naked axon can be re-covered by new myelin.
This process is called remyelination and is associated with functional recovery Franklin and ffrench-Constant The myelin sheaths generated during remyelination are typically thinner and shorter than those generated during developmental myelination.
In some circumstances, however, remyelination fails, leaving axons and even the entire neuron vulnerable to degeneration.
Thus, patients with demyelinating diseases suffer from various neurological symptoms. The representative demyelinating disease , and perhaps the most well known, is multiple sclerosis MS.
This autoimmune neurological disorder is caused by the spreading of demyelinating CNS lesions in the entire brain and over time Siffrin et al.
Patients with MS develop various symptoms, including visual loss, cognitive dysfunction, motor weakness, and pain. Approximately 80 percent of patients experience relapse and remitting episodes of neurologic deficits in the early phase of the disease relapse-remitting MS. There are no clinical deteriorations between two episodes.
Approximately ten years after disease onset, about one-half of MS patients suffer from progressive neurological deterioration secondary progressive MS. About 10—15 percent of patients never experience relapsing-remitting episodes; their neurological status deteriorates continuously without any improvement primary progressive MS. CNS myelin is produced by special cells called oligodendrocytes. PNS myelin is produced by Schwann cells.
The two types of myelin are chemically different, but they both perform the same function — to promote efficient transmission of a nerve impulse along the axon. In MS, an abnormal immune system response produces inflammation in the central nervous system. This process:. Scientists have discovered that the body heals some lesions naturally by stimulating oligodendrocytes in the area — or by recruiting young oligodendrocytes from further away — to begin making new myelin at the damaged site.
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