The functional unit of the central nervous system (CNS) is the neuron. Ultimately, general anesthetics must disrupt the function of neurons mediating behavior, consciousness, and memory. Anesthetics could accomplish this by altering the intrinsic firing rate of individual neurons (neuronal excitability) or by altering communication between neurons (synaptic transmission).

1. Neuronal Excitability. Anesthetics can hyperpolarize (create a more negative resting membrane potential) both spinal motor neurons and cortical neurons; this ability to hyperpolarize neurons correlates with anesthetic potency. Although current data still support the prevailing view that neuronal excitability is only slightly affected by general anesthetics, this small effect may nevertheless contribute significantly to the clinical actions of volatile anesthetics.
2. Synaptic Transmission. Synaptic transmission is widely considered to be the most likely subcellular site of general anesthetic action. Neurotransmission across both excitatory (not all excitatory synapses are equally sensitive to anesthetics) and inhibitory synapses is markedly altered by general anesthetics.
   1. Presynaptic Effects. Neurotransmitter release from glutamatergic synapses has consistently been found to be inhibited by clinical concentrations of volatile anesthetics.
   2. Postsynaptic Effects. Anesthetics alter the postsynaptic response to released neurotransmitters at a variety of synapses.

Mechanisms of Anesthesia and Consciousness

1. What is Anesthesia?
2. How is Anesthesia Measured?
3. What is the Chemical Nature of Anesthetic Target Sites?
4. How do Anesthetics Interfere with the Electrophysiologic Function of the Nervous System?
5. Anesthetic Actions on Ion Channels
6. How are the Molecular Effects of Anesthetics Linked to Anesthesia in the Intact Organism?
7. Where in the Central Nervous System Do Anesthetics Work?
8. Conclusions