The brain processes and transmits information using electrochemical signaling, often called electrical activity. This process manages the movement of charged particles across cell membranes, rather than generating electricity like a power plant. The controlled flow of these ions creates transient voltage changes that serve as the fundamental language of the nervous system. Understanding this requires examining the specialized cells and mechanisms they use to create, maintain, and transmit these signals.
The Neuron: The Brain’s Communicator
The neuron, or nerve cell, is the specialized unit designed to handle electrochemical communication. Each neuron possesses a distinct structure that supports receiving, integrating, and sending information. The cell body, known as the soma, houses the nucleus and machinery necessary for cellular maintenance and signal integration.
Extending from the soma are fine, branching structures called dendrites, which receive signals from thousands of other neurons. The axon is a long, slender projection that transmits the electrical impulse away from the cell body. Axon terminals interface with subsequent neurons, completing the circuit of information flow.
Maintaining the Charge: The Resting Potential
Before a signal can be sent, the neuron must establish an electrical gradient across its membrane, known as the resting potential. This potential energy is achieved by creating an imbalance of charged ions between the inside and outside of the cell. In its resting state, the inside of the neuron is negatively charged compared to the outside, maintaining a voltage difference of about -70 millivolts.
This negative charge is actively maintained by the sodium-potassium pump, a protein complex embedded in the cell membrane. The pump works against concentration gradients by expending metabolic energy to exchange ions. It pumps three positive sodium ions (\(\text{Na}^{+}\)) out of the cell for every two positive potassium ions (\(\text{K}^{+}\)) it brings in.
This unequal exchange results in a net loss of positive charge inside the cell, contributing to the negative resting potential. The neuronal membrane is also far more permeable to potassium ions through specialized leak channels than to sodium ions. As potassium ions leak out, they further increase the negative charge inside, preparing the neuron to fire its signal.
Generating the Pulse: The Action Potential
The electrical signal is a rapid, momentary reversal of the resting charge, known as an action potential. This pulse is an “all-or-nothing” event. If electrical stimulation crosses the threshold (around -55 millivolts), a full action potential fires, proceeding to the same peak voltage regardless of the initial stimulus strength.
The initial phase, called depolarization, begins with the sudden opening of voltage-gated sodium channels. Since sodium ion concentration is much higher outside the cell, they rush inward, carrying a positive charge. This rapid influx of positive sodium ions causes the internal charge to switch from negative to positive, spiking the membrane potential to a peak of about +30 millivolts.
Depolarization is immediately followed by repolarization, which restores the negative charge. Voltage-gated sodium channels quickly close, stopping the positive ion influx. Simultaneously, voltage-gated potassium channels open, allowing potassium ions to rush out of the cell, reversing the charge back toward the resting potential. This efflux often causes a brief overshoot, or hyperpolarization, making the inside of the cell more negative than its resting state before the baseline is re-established.
Bridging the Gap: Synaptic Transmission
Once generated, the action potential travels rapidly down the axon until it reaches the terminal, where it must cross a tiny gap called the synapse. Here, the signal transitions from electrical to chemical. The arrival of the electrical impulse triggers the opening of voltage-gated calcium channels.
The influx of calcium ions (\(\text{Ca}^{2+}\)) prompts small, membrane-bound sacs called synaptic vesicles to fuse with the presynaptic membrane. These vesicles release chemical messengers, known as neurotransmitters, into the synaptic cleft. The neurotransmitters diffuse across the narrow gap and bind to specific receptor proteins on the postsynaptic neuron.
Binding the neurotransmitter causes ion channels on the postsynaptic membrane to open, changing the receiving neuron’s membrane potential. This change—either encouraging or inhibiting a new action potential—converts the chemical signal back into an electrical signal. This final electrical change, the post-synaptic potential, determines whether the message will be propagated to the next cell.