Neuronal Anatomy, Membrane Potential, and Action Potential Basics
Dendrites are branching extensions that receive chemical signals through neurotransmitters. The soma, or cell body, houses the nucleus and the bulk of the organelles needed for cellular maintenance. Extending from the soma, the axon conducts electrical signals and is intermittently wrapped in fatty myelin produced by glial cells.
Resting Membrane Potential
A neuron at rest maintains an electrical gradient of roughly –65 mV relative to the extracellular space. Sodium (Na⁺), chloride (Cl⁻), and calcium (Ca²⁺) are more concentrated outside the membrane, while potassium (K⁺) and large anions (A⁻) dominate the interior. This ion distribution, together with selective membrane permeability, creates the stable resting potential.
Synaptic Potentials (EPSP/IPSP)
When neurotransmitters bind to ligand‑gated ion channels on dendrites, the channels open in response to the ligand. An influx of positive ions such as Na⁺ depolarizes the membrane, producing an excitatory postsynaptic potential (EPSP). Conversely, the influx of negative ions like Cl⁻ hyperpolarizes the membrane, generating an inhibitory postsynaptic potential (IPSP) that moves the cell toward repolarization.
The Action Potential Cycle
If the combined EPSPs raise the membrane voltage to the threshold of about –55 mV, voltage‑gated Na⁺ channels at the axon hillock open, allowing Na⁺ to rush in and drive the potential up to +40 mV. Shortly after opening, an inactivation gate blocks further Na⁺ influx. Voltage‑gated K⁺ channels then open more slowly, permitting K⁺ to exit and begin repolarizing the membrane. The sodium‑potassium pump restores ion balance by moving three Na⁺ out and two K⁺ in. During the absolute refractory period, Na⁺ channels remain inactivated; during the relative refractory period, the membrane is hyperpolarized and requires a stronger stimulus to fire again.
Signal Propagation and Myelination
Myelin sheaths, formed by Schwann cells in the peripheral nervous system or oligodendrocytes in the central nervous system, insulate the axon and leave periodic gaps called nodes of Ranvier. Voltage‑gated ion channels cluster at these nodes. In saltatory conduction, the depolarizing current “jumps” from node to node, displacing internal positive ions and dramatically accelerating transmission—up to 100 m meters per second. This mechanism makes the action potential appear to leap along the axon.
Takeaways
- Dendrites receive neurotransmitter signals, the soma houses the nucleus, and the myelinated axon conducts electrical impulses.
- A resting neuron maintains a –65 mV membrane potential through unequal ion concentrations across the membrane.
- Excitatory and inhibitory postsynaptic potentials arise from ligand‑gated ion channels that depolarize or hyperpolarize the membrane.
- When the threshold of –55 mV is reached, voltage‑gated Na⁺ channels trigger a rapid depolarization followed by K⁺‑mediated repolarization and refractory periods.
- Myelin and nodes of Ranvier enable saltatory conduction, allowing action potentials to travel up to 100 m/s by jumping between nodes.
Frequently Asked Questions
What is the threshold potential that triggers an action potential?
The threshold potential is approximately –55 mV. When combined excitatory inputs raise the membrane voltage to this level, voltage‑gated sodium channels open, initiating the rapid depolarization that defines an action potential.
How does myelin increase the speed of signal transmission?
Myelin insulates the axon and forces the depolarizing current to travel between nodes of Ranvier, a process called saltatory conduction. By jumping from node to node, the electrical signal moves far faster than continuous conduction, reaching speeds up to 100 m/s.
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