Theme C: Interaction and Interdependence · Standard & Higher Level
The nervous system represents one of the most remarkable evolutionary adaptations, allowing organisms to dynamically interact with their rapidly changing environment. At the core of this system is the neuron—a highly specialized cell adapted for transmitting electrical impulses at immense speeds across the body. The nervous system acts as the body's primary control and communication center.
Neurons possess distinct structural adaptations that align directly with their function of signal transmission:
Neurons are excitable cells, meaning they can change their membrane potential to conduct signals. When a neuron is at rest—not actively transmitting an impulse—it maintains a stable baseline charge difference across its plasma membrane. This state is known as the resting potential.
The resting potential is approximately $-70\text{ mV}$, indicating that the intracellular environment of the neuron is significantly more negative compared to the extracellular fluid.
Maintaining this unequal distribution of ions is an active process that requires a continuous supply of metabolic energy (ATP). The primary mechanisms involve:
(Replace with actual graph showing mV vs time for an action potential)
An action potential is a rapid, transient, and self-propagating electrical signal that travels along the axon of a neuron. It involves a massive, temporary disruption to the resting potential. This process is orchestrated by the precise opening and closing of voltage-gated ion channels in response to changes in membrane potential.
When a stimulus reaches the threshold potential, voltage-gated Na⁺ channels rapidly open. Na⁺ ions rush into the cell driven by both their concentration and electrical gradients. The sudden influx of positive ions reverses the membrane potential, shooting it from $-70\text{ mV}$ up to approximately $+30\text{ mV}$. The inside of the cell briefly becomes positive relative to the outside.
Almost immediately after opening, Na⁺ channels automatically close and inactivate. Simultaneously, voltage-gated K⁺ channels open. K⁺ ions rush out of the cell down their electrochemical gradient. The efflux of positive charge rapidly restores the negative internal potential, dropping it back below the resting state (a phase called hyperpolarization) before the Na⁺/K⁺ pump ultimately restores the $-70\text{ mV}$ resting baseline.
Analysis of oscilloscope traces showing resting potentials and action potentials. You must be able to identify resting potential, threshold potential, depolarization, repolarization, and hyperpolarization on a graph of membrane potential over time.
An action potential is a localized event. For a signal to travel from the brain to a muscle, the action potential must be propagated (transmitted) along the entire length of the axon without losing strength. This process is essentially a chain reaction.
Understanding threshold potentials. An action potential is strictly an "all-or-nothing" response. A stimulus must depolarize the membrane to a critical threshold (approx. $-55\text{ mV}$) to trigger the opening of voltage-gated channels. Stimuli below this threshold will not produce an action potential, regardless of their intensity. Once triggered, all action potentials have the same magnitude (up to $+30\text{ mV}$).
In vertebrates, many axons are coated with a myelin sheath, a multi-layered lipid and protein covering produced by specialized glial cells (Schwann cells in the peripheral nervous system and oligodendrocytes in the CNS). Myelin acts as a powerful electrical insulator.
Neurons do not physically touch each other. There is a microscopic gap called the synaptic cleft (approx. 20 nm wide) separating the presynaptic neuron from the postsynaptic cell (which can be another neuron, a muscle fibre, or a gland cell). Electrical impulses cannot cross this physical gap.
To overcome this, electrical signals must be transduced into a chemical message. The signaling molecules responsible for this are called neurotransmitters.
The binding of neurotransmitters to postsynaptic receptors triggers a localized change in the postsynaptic membrane potential by opening ligand-gated ion channels. The effect can be either excitatory or inhibitory, depending on the specific neurotransmitter and receptor type.
Binding of the neurotransmitter causes the opening of Na⁺ channels. The influx of positive sodium ions leads to a localized depolarization. This pushes the membrane closer to the threshold potential, increasing the likelihood that an action potential will be generated in the postsynaptic neuron.
Binding of the neurotransmitter causes the opening of K⁺ or Cl⁻ channels. K⁺ flows out or Cl⁻ flows in, leading to localized hyperpolarization. This pushes the membrane further away from the threshold potential, decreasing the likelihood of firing an action potential.
To ensure that the signal does not persist indefinitely, the neurotransmitter must be rapidly removed from the synaptic cleft shortly after release. This is achieved via enzymatic degradation (e.g., acetylcholinesterase breaking down acetylcholine) or via reuptake pumps on the presynaptic membrane.
Secretion and reabsorption of acetylcholine by neurons at synapses. Acetylcholine (ACh) is a widespread neurotransmitter. After binding, it is broken down into acetate and choline. Neonicotinoid pesticides are synthetic compounds that bind irreversibly to acetylcholine receptors in the central nervous system of insects. Because they cannot be broken down by acetylcholinesterase, they cause continuous synaptic transmission, leading to paralysis and death. They are widely used as insecticides.
It actively transports 3 Na⁺ ions out of the cell and 2 K⁺ ions into the cell using ATP. This maintains the electrochemical gradients and the negative internal charge (resting potential of approx -70 mV) necessary for the cell to be excitable.
When the threshold potential is reached, voltage-gated Na⁺ channels open. Sodium ions rush into the axon down their concentration gradient, causing the membrane potential to rapidly rise from negative (approx -70 mV) to positive (approx +30 mV).
The region of the axon that just generated an action potential enters a refractory period where its voltage-gated Na⁺ channels are temporarily inactivated. Therefore, local currents can only trigger depolarization in the forward, resting segment of the axon.
In myelinated axons, the myelin sheath insulates the membrane. Action potentials can only occur at the unmyelinated nodes of Ranvier. The electrical impulse "jumps" from node to node, which greatly increases the speed of transmission and reduces energy expenditure.
An arriving action potential triggers Ca²⁺ influx in the presynaptic knob. This causes synaptic vesicles to fuse with the membrane, releasing neurotransmitters via exocytosis. The neurotransmitters diffuse across the cleft and bind to receptors on the postsynaptic membrane, opening ion channels.
You have successfully reviewed all SL and HL understandings for Biology Theme C2.2.