Neurons are the fundamental cells of the nervous system, forming an intricate network that underlies all bodily functions. These specialized cells communicate through electrical signals, allowing for rapid information transfer throughout the brain and body. This communication is foundational to everything from simple reflexes to complex thought processes and sensory perception. Understanding how these signals are generated and transmitted provides insight into the nervous system’s operations.
The Neuron’s Resting State
A neuron at rest maintains an electrical charge difference across its membrane, known as the resting membrane potential. This potential is around -70 millivolts (mV), meaning the inside of the neuron is more negatively charged compared to the outside. This charge separation is established by the uneven distribution of various ions, including sodium (Na+), potassium (K+), chloride (Cl-), and negatively charged proteins.
The neuron’s membrane has different permeabilities to these ions due to specialized protein channels. At rest, the membrane is more permeable to potassium ions, which tend to leak out of the cell down their concentration gradient. This outward movement of positive potassium ions contributes to the negative charge inside the cell. The sodium-potassium pump actively transports three sodium ions out of the cell for every two potassium ions pumped in, further maintaining these concentration gradients and contributing to the negative resting potential.
How Neurons Fire: The Action Potential
A neuron fires by generating an action potential, a rapid change in its membrane potential. This electrical impulse begins when a stimulus causes the neuron’s membrane potential to become less negative, moving from the resting potential of -70mV towards a threshold voltage, around -55mV. If this threshold is reached, voltage-gated sodium channels open rapidly.
The opening of these sodium channels allows an influx of positively charged sodium ions into the cell, causing the inside of the neuron to become positively charged, a phase known as depolarization. This positive shift can reach up to +30mV. Following depolarization, voltage-gated sodium channels inactivate, and voltage-gated potassium channels open, allowing potassium ions to flow out of the cell.
The outflow of positive potassium ions rapidly restores the negative charge inside the cell, a process called repolarization. Potassium channels may remain open longer, causing a brief period where the membrane potential becomes even more negative than the resting potential, known as hyperpolarization. This “all-or-none” principle means that once the threshold is reached, an action potential of a consistent magnitude will be generated, regardless of the stimulus strength.
Sending the Signal Down the Line
Once an action potential is generated, it travels along the axon, the long projection extending from the neuron’s cell body. This propagation involves the action potential regenerating itself at successive points. The influx of sodium ions during depolarization at one point creates local currents that depolarize the adjacent membrane segment, triggering new voltage-gated sodium channels to open.
Many axons are covered by a myelin sheath, a fatty insulating layer formed by glial cells. This myelin sheath is interrupted at regular intervals by small gaps called Nodes of Ranvier. These nodes are rich in voltage-gated sodium and potassium channels. In myelinated axons, the action potential appears to “jump” from one Node of Ranvier to the next, a process called saltatory conduction.
Saltatory conduction increases the speed of signal transmission, allowing impulses to travel faster than in unmyelinated axons. This jumping mechanism also conserves energy for the neuron, as ion channels only need to operate at the nodes. In unmyelinated axons, conduction is continuous but slower, as the action potential must be re-established at every point along the axon.
Neurons Talking to Each Other: Synapses
Neurons communicate with each other at specialized junctions called synapses. At a chemical synapse, the signal is transmitted from a presynaptic neuron to a postsynaptic neuron without direct electrical contact. The two neurons are separated by a tiny gap called the synaptic cleft, 20-40 nanometers wide.
When an action potential arrives at the axon terminal of the presynaptic neuron, it triggers the release of chemical messengers called neurotransmitters. These neurotransmitters are stored in small sacs called synaptic vesicles and are released into the synaptic cleft through exocytosis. The released neurotransmitters then diffuse across the synaptic cleft and bind to specific receptor proteins on the membrane of the postsynaptic neuron.
The binding of neurotransmitters to their receptors causes ion channels on the postsynaptic membrane to open or close, leading to a change in the postsynaptic neuron’s membrane potential. This change can be either excitatory (making the postsynaptic neuron more likely to fire an action potential) or inhibitory (making it less likely to fire). The effect depends on the specific neurotransmitter and the type of receptor it binds to.
The Brain’s Electrical Symphony
The coordinated electrical signals within neurons form the basis of all brain functions. The rapid firing and intricate communication between countless neurons underpin processes such as thought, memory formation, emotions, and sensory perception. This constant exchange of messages, known as neurotransmission, allows the nervous system to act as the body’s command center, regulating both conscious actions and involuntary functions like breathing and heart rate.
Disruptions in electrical signaling can lead to neurological disorders. For instance, abnormal surges in electrical activity in the brain can cause recurring seizures, as seen in epilepsy. Conditions like Parkinson’s disease and depression are linked to imbalances or disruptions in specific neurotransmitter systems and the electrical circuits they form. Understanding these electrical processes is important for developing treatments and interventions for such conditions.