General anesthetics produce two important physiologic effects at the cellular level. First, inhala-tional anesthetics hyperpolarize neurons, possibly an important effect on neurons serving a pacemaker role and on pattern-generating circuits and in synaptic communication, since reduced excitability in a postsynaptic neuron diminishes the likelihood that an action potential will be initiated in response to neurotransmitter release. Second, at anesthetizing concentrations, both inhala-tional and intravenous anesthetics have substantial effects on synaptic transmission and much smaller effects on action-potential generation or propagation. Inhalational anesthetics inhibit excitatory synapses and enhance inhibitory synapses via effects on pre- and postsynaptic sites. The inhalational anesthetic isoflurane clearly can inhibit neurotransmitter release and produce a small reduction in presynaptic action potential amplitude (3% reduction at MAC concentration) that inhibits neurotransmitter release, a significant effect because the reduced action potential is amplified into a larger reduction in presynaptic Ca2+ influx, and thence into an even greater reduction in transmitter release. Inhalational anesthetics also can act postsynaptically, to alter the response to released neurotransmitter, probably via actions at neurotransmitter receptors.
Intravenous anesthetics produce a narrower range of physiological effects, predominantly at the synapse, where they have profound and relatively specific effects on the postsynaptic response to released neurotransmitter. Most of the intravenous agents act predominantly by enhancing inhibitory neurotransmission, whereas ketamine predominantly inhibits excitatory neurotransmission at glutamatergic synapses.
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