Action Potentials and Synaptic Transmission in the Nervous System

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Action Potentials

Overview of Action Potentials

Action potentials (APs) are the principal mechanism by which neurons communicate over long distances. They are rapid, transient changes in membrane potential that occur only in muscle cells and axons of neurons. Unlike graded potentials, action potentials do not decay over distance and are also referred to as nerve impulses in neurons. The process involves the opening and closing of specific voltage-gated ion channels.

Key Point: Action potentials are essential for neural communication and muscle contraction.
Key Point: APs involve a brief reversal of membrane potential (~100 mV).
Key Point: APs are generated by voltage-gated sodium (Na+) and potassium (K+) channels.

Phases of the Action Potential

The generation of an action potential consists of four main steps, each involving specific ion channel activity:

Resting State

At rest, all gated Na+ and K+ channels are closed. Only leakage channels are open, maintaining the resting membrane potential (RMP). Each Na+ channel has two gates: activation (closed at rest) and inactivation (open at rest).

Key Point: The membrane is polarized, with a typical RMP of -70 mV.

Resting state: All gated Na+ and K+ channels are closed.

Depolarization

Depolarization occurs when voltage-gated Na+ channels open, allowing Na+ to enter the cell. This influx causes the membrane potential to become less negative, and if the threshold (~-55 mV) is reached, all Na+ channels open, resulting in a rapid spike to +30 mV.

Key Point: Positive feedback leads to the opening of more Na+ channels.

Depolarization: Na+ channels open, allowing Na+ entry.

Repolarization

During repolarization, Na+ channels inactivate and K+ channels open, allowing K+ to exit the cell. This restores the membrane potential toward its resting value.

Key Point: Repolarization resets electrical conditions, not ionic conditions.

Repolarization: Na+ channels are inactivating, K+ channels open, allowing K+ to exit.

Hyperpolarization

Some K+ channels remain open, causing excessive K+ efflux and making the membrane potential more negative than the resting state. Na+ channels begin to reset.

Key Point: Hyperpolarization is a slight dip below the resting voltage.

Hyperpolarization: Some K+ channels remain open, and Na+ channels reset.

Propagation of Action Potentials

Once initiated, an action potential is self-propagating and moves in a forward direction along the axon. In nonmyelinated axons, each segment depolarizes and repolarizes sequentially. In myelinated axons, propagation is faster due to saltatory conduction, where the AP jumps from one node of Ranvier to another.

Key Point: APs are transmitted from the origin down the entire axon length toward terminals.

Propagation of an action potential along an axon.

Threshold and All-or-None Phenomenon

For an action potential to occur, depolarization must reach a threshold voltage. If threshold is reached, the AP occurs completely; if not, it does not occur at all. This is known as the all-or-none phenomenon.

Key Point: APs are independent of stimulus intensity; stronger stimuli increase AP frequency, not amplitude.

Relationship between stimulus strength and action potential frequency.

Refractory Periods

The refractory period is the time during which a neuron cannot trigger another action potential. It is divided into absolute and relative refractory periods. During the absolute refractory period, Na+ channels are open or inactivated, preventing another AP. During the relative refractory period, a stronger stimulus can initiate another AP.

Key Point: Refractory periods ensure unidirectional propagation and limit AP frequency.

$Absolute and relative refractory periods in an action potential.$

Conduction Velocity

The speed of AP conduction depends on axon diameter and degree of myelination. Larger diameter fibers conduct faster due to less resistance. Myelinated axons use saltatory conduction, which is much faster than continuous conduction in nonmyelinated axons.

Key Point: Myelin sheaths insulate axons and allow rapid AP transmission.

Clinical Relevance

Multiple sclerosis (MS) is an autoimmune disease that damages myelin, impairing AP propagation. Local anesthetics like lidocaine block voltage-gated Na+ channels, preventing AP generation.

Synaptic Transmission

The Synapse

Synapses are junctions that mediate information transfer from one neuron to another or to an effector cell. The presynaptic neuron sends information, while the postsynaptic neuron receives it. Synaptic connections can be axodendritic, axosomatic, axoaxonal, dendrodendritic, or somatodendritic.

Key Point: Synapses are essential for neural networks and information processing.

Types of synaptic connections in a neuron.

Types of Synapses

Electrical Synapses

Electrical synapses are less common and involve direct cytoplasmic connections via gap junctions. They allow rapid, bidirectional communication and are abundant in embryonic nervous tissue and certain brain regions.

Chemical Synapses

Chemical synapses are specialized for the release and reception of neurotransmitters. The axon terminal of the presynaptic neuron contains synaptic vesicles, while the postsynaptic membrane has receptor regions. The synaptic cleft separates the two, and transmission involves neurotransmitter release, diffusion, and receptor binding.

Key Point: Chemical synapses ensure unidirectional communication and are the most common type.

Transmission Across Chemical Synapses

AP arrives at axon terminal.
Voltage-gated Ca2+ channels open, Ca2+ enters axon.
Ca2+ induces synaptic vesicles to release neurotransmitter by exocytosis.
Neurotransmitter diffuses across synaptic cleft and binds to receptors on target cell.
Ion channels open in target cell.
Neurotransmitter is broken down.

Postsynaptic Potentials

Excitatory and Inhibitory Postsynaptic Potentials

Neurotransmitter binding causes graded potentials in the postsynaptic neuron. Excitatory postsynaptic potentials (EPSPs) result from Na+ influx, causing depolarization. Inhibitory postsynaptic potentials (IPSPs) result from K+ or Cl- movement, causing hyperpolarization.

Key Point: EPSPs can trigger APs if they reach threshold; IPSPs move the membrane potential farther from threshold.

Summation and Integration

EPSPs and IPSPs can summate to influence the postsynaptic neuron. Only if EPSPs predominate and bring the axon hillock to threshold will an AP be generated.

Neurotransmitters

Classification by Chemical Structure

Biogenic amines: Dopamine, norepinephrine, epinephrine, serotonin, histamine.
Acetylcholine (ACh): Released at neuromuscular junctions, degraded by acetylcholinesterase.

Classification by Function

Effects: Excitatory (depolarizing) or inhibitory (hyperpolarizing), depending on receptor type.
Actions: Direct (binds and opens ion channels) or indirect (acts through second messengers).

Neurotransmitter Receptors

Channel-linked receptors: Ligand-gated ion channels, immediate and brief action.
G protein–linked receptors: Indirect, complex, slow, and prolonged responses.

Neuromodulators

Neuromodulators are chemical messengers that affect the strength of synaptic transmission without directly causing EPSPs or IPSPs. They may influence neurotransmitter synthesis, release, degradation, or reuptake, and alter postsynaptic membrane sensitivity.

Clinical Terms

Neuropathy: Disease or dysfunction of one or more peripheral nerves.
Neurotoxin: Substance that damages or destroys nerve tissue.
Rabies: Viral disease causing inflammation of the brain.
Shingles: Viral infection causing painful rash, affecting nerve tissue.

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