Myelin, Conduction, Regeneration, and Electrophysiology

Myelin sheath

Insulation around the axon; increases action potential conduction velocity; 20% protein, 80% lipid

Myelin sheath forms

Formed by oligodendrocytes in CNS; Schwann cells in PNS

Myelination

Begins at week 14 of fetal development; proceeds rapidly during infancy; completed in late adolescence; dietary fat important

Schwann cells in PNS

Each cell spirals repeatedly around a small section of a single axon

Neurilemma

Thick, outermost coil of myelin sheath

Oligodendrocytes in CNS

Produce myelin

Nodes of Ranvier

Gaps between myelinated segments

Internodes

Myelin-covered segments

Trigger zone

Axon hillock and initial segment where action potentials begin

Multiple Sclerosis

Disease of myelin sheath; myelin replaced by scar tissue; nerve conduction disrupted; double vision, tremors, numbness, speech defects; onset 20–40

Tay-Sachs

Disease of myelin sheath; hereditary; infants of Eastern European Jewish descent; fatal before 4; blindness, loss of coordination, dementia

Unmyelinated axons

Slower signal conduction compared to myelinated axons

Conduction velocity

Depends on axon diameter and presence/absence of myelin

Conduction speed

Small, unmyelinated: 0.5–2 m/s; small, lightly myelinated: 3–15 m/s; large, myelinated: up to 120 m/s

Large axons

Large soma and energy required to maintain

Brain tumors arise from

Meninges, metastasis from other organs, glial cells (mitotically active)

Gliomas

Grow rapidly, highly malignant; blood-brain barrier reduces chemo effectiveness

Nerve regeneration

Possible in PNS if soma intact and some neurilemma remains

Steps of regeneration

1) Axon distal degenerates; macrophages clean debris; 2) Soma swells, ER breaks up, nucleus moves; 3) Axon stump sprouts; 4) Schwann cells, basal lamina, neurilemma form regeneration tube

Nerve growth factor

Protein secreted by gland, muscle, or glial cells; picked up by axon terminals

Electrophysiology

Study of cellular mechanisms for producing electrical signals

Electrical potential

Difference in electrical charge (electrical gradient) between two points

Membrane potential

Caused by separation of ions across the cell membrane

Electrical current

Flow of charged particles due to a voltage difference

Resting membrane potential

Voltage across membrane when neuron is “at rest”

Ion channels

Selectively permeable; K+ channels allow K+ only; Na+ channels allow Na+ only

Ionic current determined by

Ion concentration gradient and electrical gradient (membrane potential)

Na/K Pump

Moves Na+ out, K+ in; requires ATP; maintains concentration gradients

Depolarization

Shift in membrane potential to a less negative value

Hyperpolarization

Shift in membrane potential to a more negative value

Local potential

Change in membrane potential at/near stimulation point; can be depolarization or hyperpolarization

Properties of local potentials

Graded, decremental, reversible

Graded

Vary in magnitude with stimulus strength

Decremental

Get weaker as they spread from the stimulation point

Reversible

If stimulation ceases, membrane returns to resting potential

Action potential

Rapid up-and-down shift in membrane potential; can travel long distance

Sensory neurons stimulated by

Chemicals, light, heat, or mechanical disturbance

Action potentials produced by

Coordinated opening/closing of voltage-gated ion channels

Action potential phases

Depolarization, Repolarization, Hyperpolarization

Depolarization

Voltage-gated Na+ channels open rapidly; Na+ enters

Repolarization

Voltage-gated Na+ channels inactivate; K+ channels open; K+ exits

Hyperpolarization

Membrane more negative than resting; K+ permeability higher than rest; Na+ permeability lower than rest

Action potential characteristics

All-or-none, nondecremental, irreversible

Refractory period

Time during and after AP when another AP is difficult/impossible

Absolute refractory period

No stimulus can trigger another AP; caused by inactivated Na+ channels

Relative refractory period

Stronger stimulus needed to trigger AP; occurs during hyperpolarization

Unmyelinated axons

Voltage-gated channels along entire length

Trigger zone AP

Causes Na+ to enter axon and diffuse into adjacent regions

Na+ diffusion effect

Depolarizes nearby membrane

Depolarization

Opens voltage-gated ion channels

Opening voltage-gated channels

Produces new AP

New AP

Allows Na+ to diffuse to next distal segment

Signal propagation in unmyelinated axons

Chain reaction down the axon

Continuous conduction

Signal transmission along unmyelinated axons

Continuous conduction analogy

Like a wave of falling dominoes

Saltatory conduction

Signal conduction in myelinated axons; appears to jump from node to node

Saltatory conduction pattern

Faster due to myelin insulation

Nodes of Ranvier

Bare axon segments where AP generated

AP generation

Occurs only at nodes of Ranvier

Voltage-gated channels

Concentrated at nodes

Myelinated internodes

Few/no voltage-gated channels

Passive spread

Signal decreases in strength like local potential

Signal at next node

Strong enough to reach threshold

Threshold at node

Opens voltage-gated Na+ channels

New AP at node

Full-strength AP generated