The nervous system relies on specialized cells called neurons to transmit information throughout the body. A neuron is the basic signaling unit, capable of conducting an electrical impulse from its cell body down a slender extension called the axon. For this signal to move from one neuron to the next, it must cross a tiny physical gap known as the synapse. This junction is where the electrical signal is temporarily converted into a chemical message, which then travels across the gap to activate the receiving cell. This conversion process, known as synaptic transmission, ensures that signals are passed accurately and rapidly across the nervous system’s vast network.
The Signal Arrives
The initial phase of communication begins when the action potential travels along the axon of the sending neuron. This wave of electrical charge moves swiftly down the length of the axon until it reaches the axon terminal, the specialized structure that forms one half of the synapse. This electrical pulse is a temporary, rapid shift in the voltage across the neuron’s cell membrane.
The electrical signal cannot simply jump the synaptic cleft, the physical space separating the two neurons. Instead, the signal halts at the membrane of the presynaptic terminal. The arrival of the action potential is the specific trigger required to transition the communication from an electrical form into a chemical one.
Releasing the Chemical Message
The change in membrane voltage caused by the arriving action potential causes specialized voltage-gated calcium channels to open. When the channels open, there is a rapid influx of positively charged calcium ions (\(\text{Ca}^{2+}\)) from the extracellular fluid into the neuron’s terminal.
This surge of calcium ions acts as the internal signal that triggers the release of the chemical message. Within the presynaptic terminal are synaptic vesicles, small membrane-bound sacs filled with neurotransmitters. The calcium ions bind to specific sensor proteins associated with the vesicles.
The binding of calcium initiates a mechanical process that compels the vesicles to merge with the presynaptic cell membrane. This fusion process, called exocytosis, allows the neurotransmitters to spill into the synaptic cleft. The entire release occurs with remarkable speed.
Decoding the Message
Once released, the neurotransmitter molecules quickly diffuse across the narrow synaptic cleft. On the membrane of the postsynaptic neuron, they encounter specific receptor proteins designed to recognize them. This binding acts like a key fitting into a lock, instantly translating the chemical signal back into an electrical one, and the postsynaptic neuron employs two primary types of receptors to decode this message.
Ionotropic Receptors
Ionotropic receptors, also called ligand-gated ion channels, are fast-acting because they contain both the binding site and the ion channel within a single protein structure. When the neurotransmitter binds, the channel opens immediately, allowing ions like sodium (\(\text{Na}^{+}\)) or chloride (\(\text{Cl}^{-}\)) to flow directly into the cell.
The resulting ion flow rapidly changes the electrical potential of the postsynaptic neuron. If the incoming ions cause the cell’s voltage to become more positive, it creates an Excitatory Postsynaptic Potential (EPSP), increasing the likelihood of the receiving neuron generating its own action potential. Conversely, if the ion flow causes the cell’s voltage to become more negative, it produces an Inhibitory Postsynaptic Potential (IPSP), which suppresses the cell’s activity.
Metabotropic Receptors
Metabotropic receptors, often called G-protein coupled receptors, act more slowly. These receptors do not directly form an ion channel; instead, binding a neurotransmitter activates an internal G-protein. This activated G-protein then initiates a cascade of intracellular events, which may eventually lead to the opening or closing of ion channels located elsewhere on the membrane.
Because this process involves multiple biochemical steps, the effects of metabotropic receptors are slower to begin but can last much longer. The ultimate effect of either receptor type, whether excitation or inhibition, determines if the signal is successfully passed along the neural circuit.
Clearing the Synapse
For the nervous system to function efficiently, the chemical message must not linger in the synaptic cleft, or the receiving neuron would be continuously activated. The signal must be terminated rapidly to reset the synapse for the next incoming action potential. This clearance is achieved through three primary mechanisms.
Reuptake
Reuptake involves specialized transporter proteins embedded in the presynaptic membrane actively pumping the released neurotransmitter molecules back into the sending neuron. This recycling process is used for many small-molecule neurotransmitters, such as serotonin and dopamine, and is crucial for maintaining the neuron’s supply.
Enzymatic Degradation
Enzymatic degradation occurs when specific enzymes located within the synaptic cleft break down the neurotransmitter into inactive fragments. A classic example is the enzyme acetylcholinesterase, which rapidly degrades the neurotransmitter acetylcholine, ensuring a quick cessation of the signal at the synapse.
Diffusion
A certain amount of neurotransmitter simply dissipates through diffusion, drifting away from the receptors and out of the synaptic cleft. This passive process, combined with the other active mechanisms, ensures the transient nature of the chemical signal.