Anesthesia generally works by disrupting the communication between nerve cells (neurons) in your brain and spinal cord, effectively 'turning down' or blocking signals related to consciousness, pain, and movement.
How Anesthetics Affect Neurons
Nerve cells communicate with each other at tiny junctions called synapses. When one neuron wants to send a message to another, it releases chemical messengers called neurotransmitters into the synapse. These neurotransmitters then bind to receptors on the receiving neuron, triggering a response.
General anesthetics interfere with this signaling process in several ways. They can enhance the activity of inhibitory neurotransmitters (like GABA), making neurons less likely to fire, or they can inhibit the activity of excitatory neurotransmitters (like glutamate), preventing neurons from sending signals.
Key Mechanism: Blocking Neurotransmitter Release
One significant way general anesthetics exert their effect is by interfering with the release of these chemical messengers. Specifically, research indicates that general anesthetics, particularly, inhibit the presynaptic voltage-gated sodium channels in glutamatergic synapse, which inhibits the excitation of the neuron by blocking the release of presynaptic neurotransmitters [5,13].
Let's break that down:
- Glutamatergic synapse: A synapse where the primary excitatory neurotransmitter is glutamate. These are crucial for sending 'go' signals in the brain.
- Presynaptic: Refers to the neuron sending the signal.
- Voltage-gated sodium channels: These are tiny pores on the neuron's surface that open and close based on the electrical voltage across the cell membrane. They are essential for generating the electrical impulse (called an action potential) that travels down the neuron and triggers the release of neurotransmitters.
- Inhibition: Anesthetics block or slow down the function of these sodium channels.
By inhibiting these critical sodium channels [5,13], anesthetics prevent the electrical impulse from reaching the end of the presynaptic neuron effectively. Without this impulse, the neuron cannot release its glutamate neurotransmitters.
The Impact of Blocking Release
Imagine it like a light switch:
| Normal Nerve Signaling | Anesthetized Nerve Signaling |
|---|---|
| Electrical signal (action potential) travels down neuron | Anesthetic blocks voltage-gated sodium channels [5,13] |
| Signal reaches the end, triggering neurotransmitter release | Electrical signal is weak or blocked; neurotransmitter release inhibited [5,13] |
| Neurotransmitters activate the next neuron ('light is on') | Next neuron does not receive the 'on' signal ('light stays off') |
This blockage of excitatory neurotransmitter release [5,13], along with other effects anesthetics have on different channels and receptors, significantly reduces the overall electrical activity in the brain and spinal cord.
The Result: The Anesthetized State
This widespread dampening of nerve cell communication leads to the characteristic effects of general anesthesia:
- Unconsciousness: The brain areas responsible for awareness and consciousness are suppressed.
- Amnesia: Memory formation is impaired.
- Analgesia: Pain signals are blocked or perceived differently.
- Muscle Relaxation: Signals to muscles can be reduced.
In essence, by interfering with the fundamental process of nerve signaling, particularly by inhibiting key channels necessary for neurotransmitter release [5,13], anesthetics create a reversible state of controlled unawareness and unresponsiveness, allowing medical procedures to be performed safely.
