Neuron Anatomy Explained: Soma, Axon, Myelin Sheath | Nervous System Model

The myelin sheath is a fatty insulating layer produced by Schwann cells (peripheral nervous system) and oligodendrocytes (central nervous system). It wraps around axons and increases the speed of electrical signal transmission. Myelin acts as an insulator, allowing signals to jump between gaps called nodes of Ranvier. This saltatory conduction significantly increases the speed of nerve impulse transmission.

Myelin sheaths increase nerve impulse conduction speed through saltatory conduction. In the PNS, Schwann cells wrap around axons like hot dog buns, with gaps called nodes of Ranvier between them. In the CNS, oligodendrocytes myelinate multiple axons. At nodes of Ranvier, voltage-gated channels are concentrated. Action potentials jump from node to node rather than propagating continuously, dramatically increasing transmission speed. This mechanism is essential for rapid communication in long neurons.

Saltatory conduction is the mechanism by which action potentials 'leap' from one node of Ranvier to the next along myelinated axons. The myelin sheath, composed primarily of sphingomyelin formed by Schwann cells in the peripheral nervous system, acts as an excellent electrical insulator, reducing ionic flux by approximately 5,000 times. Since myelin prevents ion flow along most of the axon, action potentials only occur at the exposed nodes containing voltage-gated channels. This mechanism increases conduction velocity between 5 and 50 times compared to unmyelinated fibers, with maximum speeds reaching 100 meters per second.

The myelin sheath is interrupted at regular intervals by gaps called nodes of Ranvier. During saltatory conduction, action potentials jump from one node to the next rather than traveling continuously along the entire axon. This jumping mechanism dramatically increases the speed of signal transmission compared to unmyelinated axons.

At the end of the axon, there are axon terminals that release neurotransmitters into the synaptic gap (synapse) between neurons. Neurotransmitters are chemical messengers that transmit signals across the synapse to the next neuron or target cell. This chemical transmission allows signals to cross the small gap between neurons, enabling communication throughout the nervous system.

Neurons do not physically touch each other. The junction between neurons is called a synapse, with a small space called the synaptic gap. Information crosses this gap chemically through neurotransmitters, which are molecules produced and released by neurons. When an electrical impulse reaches the axon's end, it triggers neurotransmitter release into the synaptic gap. These chemicals bind to receptors on the next neuron, continuing the signal transmission.

At the end of a neuron, chemical messengers called neurotransmitters cross a tiny gap called the synapse to transmit signals to the next cell. This chemical transmission bridges the gap between neurons, enabling communication across the nervous system.

Synapses are junctions between neurons where signals are transmitted. The axon terminal releases neurotransmitters (chemical messengers) into the synaptic gap, which bind to receptors on the target cell. Neurotransmitters include acetylcholine (muscle contraction), dopamine (movement and reward), serotonin (mood), and GABA (inhibition). This chemical transmission allows precise and specific communication between cells, enabling complex nervous system functions.

Electrical impulses cannot travel directly across the gap between neurons called the synapse. Instead, neurotransmitters—chemical messengers—are released from the end of one neuron to cross the synaptic gap and bind to receptors on the next neuron, allowing the signal to continue transmitting. This chemical transmission enables information to pass between neurons despite the physical gap.

Glial cells support neurons: satellite cells (PNS) exchange substances between neurons and blood vessels; Schwann cells (PNS) and oligodendrocytes (CNS) produce myelin sheath. Cerebrospinal fluid (CSF) surrounds and protects the brain and spinal cord, providing cushioning, removing waste, and maintaining chemical balance. This support system enables efficient nervous system function.

Glial cells (10% neurons, 90% glial cells) include astrocytes (support and nourish neurons, form blood-brain barrier), microglia (immune cells that eliminate pathogens and debris), oligodendrocytes and Schwann cells (produce myelin sheath for insulation), and ependymal cells (line ventricles and allow cerebrospinal fluid movement). Myelin enables saltatory conduction, increasing speed. Schwann cells allow axon regeneration in the peripheral nervous system, while oligodendrocytes do not, preventing regeneration in the central nervous system.

Neuroglial cells (glia) are supporting cells in the nervous system: (1) Ependymal cells - produce cerebrospinal fluid, (2) Oligodendrocytes - produce myelin in the CNS, (3) Microglial cells - immune cells, (4) Schwann cells - produce myelin in the PNS, (5) Astrocytes - provide structural and metabolic support. The myelin sheath is a fatty layer that wraps around axons, produced by oligodendrocytes in the CNS and Schwann cells in the PNS.

The nervous system consists of neurons and glial cells. Glial cells protect, support, and nourish neurons. The neuroglia includes astrocytes, oligodendrocytes, Schwann cells, and microglia. Astrocytes are star-shaped cells that form the blood-brain barrier by wrapping around capillaries, controlling substance passage between blood and brain tissue. They also participate in neurotransmitter metabolism. Oligodendrocytes and Schwann cells produce myelin for efficient signal transmission; oligodendrocytes work in the CNS and can wrap around multiple axons, while Schwann cells work in the PNS and wrap around single axons. Microglia constitute 20% of glial cells and serve as the primary immune defense in the CNS, functioning like macrophages to phagocytose harmful substances and present antigens to the immune system.

Neurons are the structural and functional units of the nervous system, responsible for generating and transmitting nerve impulses. Neurons consist of the cell body (soma), dendrites (receive signals), and axons (transmit signals). Nissl bodies (ribosomes and rough endoplasmic reticulum) are found in the cell body and dendrites for protein synthesis. Glial cells (neuroglia) constitute more than 50% of the nervous system and provide structural and functional support. Types include astrocytes (support and blood-brain barrier), Schwann cells (myelin in PNS), oligodendrocytes (myelin in CNS), microglia (immune function), and ependymal cells (CSF production). Myelin sheath is a fatty insulating layer that surrounds axons and increases the speed of nerve impulse transmission. Myelin is formed by Schwann cells in the peripheral nervous system and oligodendrocytes in the central nervous system. The myelin sheath acts as an electrical insulator, allowing nerve impulses to jump between nodes of Ranvier in saltatory conduction.

Demyelination occurs when myelin sheaths are destroyed and replaced by plaques, disrupting saltatory conduction and slowing action potentials. Three major demyelinating conditions must be known: Multiple Sclerosis (autoimmune attack on CNS/PNS myelin with vision loss, weakness, fatigue, and autonomic dysfunction); Guillain-Barré Syndrome (immune-mediated peripheral neuropathy triggered by infections); and Chronic Inflammatory Demyelinating Polyneuropathy (chronic, slowly progressive form). Myelin can regenerate if the underlying nerve survives.

Demyelinating disorders destroy myelin while preserving axons. Multiple sclerosis is autoimmune with multiple demyelinating episodes disseminated in space and time, most common in young adults (20-30 years), more common in women, associated with HLA-DR2. Clinical features include optic neuritis (most common), brainstem involvement (vertigo, diplopia), and spinal cord involvement. CSF shows increased lymphocytes, immunoglobulins with clonal bands, and myelin basic proteins. Treatment includes intravenous steroids for acute attacks and interferon beta for disease progression. Progressive multifocal leukoencephalopathy is caused by JC virus infection of oligodendrocytes, presenting with progressive multifocal demyelination in immunocompromised patients. Central pontine myelinolysis results from rapid IV correction of hyponatremia, causing demyelination of pons and potentially locked-in syndrome.

Multiple sclerosis is classified as a demyelinating disease, which is an umbrella term encompassing various conditions that cause destruction of myelin. While multiple sclerosis is the most well-known and common demyelinating disease, there are many other diseases that can also cause demyelination of the nervous system.

Demyelinating diseases are acquired conditions that damage myelin while preserving axons, with clinical features resulting from impaired electrical impulse transmission. Multiple sclerosis (MS), the most common demyelinating disorder, affects 1 in 1000 people and is characterized by distinct episodes of neurological deficits separated in time and space. Women are affected twice as often as men, with geographic variation showing higher prevalence away from the equator. Pathogenesis involves T helper 1 and T helper 17 cells reacting against myelin antigens. Clinical presentations include optic neuropathy, brain stem demyelination, and spinal cord lesions. Diagnosis requires two or more attacks affecting different CNS parts, supported by MRI and CSF oligoclonal bands. Treatment includes immunosuppressive agents like beta-interferon. Other demyelinating conditions include neuromyelitis optica (aquaporin-4 antibodies), acute disseminated encephalomyelitis (post-viral), acute necrotizing hemorrhagic encephalomyelitis (fatal), and central pontine myelinolysis (osmotic demyelination syndrome from rapid sodium correction).

Demyelination is a pathological process damaging the myelin sheath covering nerve fibers. Multiple sclerosis affects 2.5 million people globally, making it the most common demyelinating disease. Other conditions include optic neuritis, transverse myelitis, and ADEM. The myelin sheath enables electrical signal transmission like cable insulation. Mild damage allows self-repair, but severe damage causes permanent nerve fiber death. Symptoms occur in patches across multiple organs: motor symptoms (35% of patients) include walking difficulties and spasms; visual symptoms (36%) include eye pain and transient vision loss; sensory symptoms (61%) include tingling sensations; mental symptoms (40%) include mild intellectual deterioration.