The phrase “neurons firing” refers to the fundamental process by which nerve cells, or neurons, generate and transmit electrical signals. This electrical activity, known as an action potential, allows neurons to communicate with each other across vast networks within the nervous system. The rapid propagation of these signals forms the basis of all brain function and enables the body to process information and respond to its environment.
The Neuron’s Resting State
Before a neuron “fires,” it exists in a baseline electrical state called the resting membrane potential. In this state, the inside of the neuron is negatively charged compared to the outside, typically around -70 millivolts (mV). This negative charge is maintained by an uneven distribution of charged particles, or ions, across the neuron’s cell membrane. Specifically, there’s a higher concentration of sodium ions (Na+) outside the cell and a higher concentration of potassium ions (K+) inside the cell.
The neuron’s membrane has specialized protein structures called ion channels and ion pumps that regulate this ion distribution. Leak channels, particularly potassium leak channels, are open during the resting state, allowing some potassium ions to slowly diffuse out of the cell. While a small amount of sodium also leaks in, the sodium-potassium pump actively works to maintain the concentration gradients by pumping three sodium ions out for every two potassium ions it brings into the cell, consuming energy in the process.
The Spark: How a Neuron Fires
The “firing” of a neuron, scientifically termed an action potential, begins when the neuron receives a stimulus that causes its internal electrical charge to rise from the resting potential. This initial change is called depolarization, where the inside of the cell becomes less negative. If this depolarization reaches a specific level, known as the threshold potential (typically around -55 mV), voltage-gated sodium channels in the neuron’s membrane rapidly open.
The opening of these sodium channels leads to a sudden, massive influx of positively charged sodium ions into the cell. This rapid inflow of positive charge causes the inside of the neuron to become significantly more positive, often reaching a peak of about +30 mV, a phase referred to as the overshoot. This dramatic shift in charge is an all-or-nothing event; once the threshold is met, the action potential fires at its full strength.
Following this rapid depolarization, the neuron begins to restore its negative charge in a process called repolarization. The voltage-gated sodium channels inactivate, effectively stopping the influx of sodium ions. Simultaneously, voltage-gated potassium channels open, allowing positively charged potassium ions to rush out of the cell. This outflow of positive charge quickly brings the membrane potential back towards its resting negative state.
Sometimes, the potassium channels remain open for a brief period longer than necessary, causing the membrane potential to become even more negative than the resting potential, a state known as hyperpolarization or undershoot. This brief period ensures that the neuron cannot fire another action potential immediately, a concept known as the refractory period. Once the potassium channels close, and with the help of the sodium-potassium pump, the neuron’s membrane potential returns to its resting state, ready for another signal.
Passing the Message: Synaptic Transmission
After a neuron generates an electrical signal, it must transmit this message to other neurons, which occurs at specialized junctions called synapses. The electrical signal, or action potential, travels down the axon of the “presynaptic” neuron until it reaches the axon terminal. At the axon terminal, the electrical signal is converted into a chemical signal.
This conversion involves the release of chemical messengers called neurotransmitters into the synaptic cleft, a tiny gap between the presynaptic neuron and the “postsynaptic” neuron. When the action potential arrives at the axon terminal, it triggers the opening of voltage-gated calcium channels, allowing calcium ions to enter the presynaptic neuron. This influx of calcium causes synaptic vesicles, which are small sacs containing neurotransmitters, to fuse with the presynaptic membrane and release their contents into the synaptic cleft.
These neurotransmitters then diffuse across the synaptic cleft and bind to specific receptor proteins located on the membrane of the postsynaptic neuron, much like a key fitting into a lock. The binding of neurotransmitters to these receptors can have two main effects on the postsynaptic neuron: excitation or inhibition. Excitatory neurotransmitters, such as glutamate, make the postsynaptic neuron more likely to fire its own action potential by causing depolarization. Conversely, inhibitory neurotransmitters, like GABA, make the postsynaptic neuron less likely to fire by causing hyperpolarization or preventing depolarization.
The Impact of Neural Firing
The continuous firing and communication between neurons form the foundation of all brain functions. This microscopic electrical and chemical signaling underlies every thought, memory, and emotion. For instance, the formation and retrieval of memories heavily rely on specific patterns of neural firing, particularly involving regions like the hippocampus. Learning and memory processes are associated with changes in the strength of these synaptic connections, influenced by repeated neural activity.
Beyond cognition, neural firing orchestrates all voluntary and involuntary movements, as motor neurons transmit signals from the brain and spinal cord to muscles, causing them to contract. Similarly, sensory perception, such as seeing, hearing, touching, tasting, and smelling, depends on sensory neurons firing in response to stimuli and sending those signals to specific areas of the brain for interpretation.