Sites Of Action

In principle, general anesthetics could interrupt nervous system function at myriad levels, including peripheral sensory neurons, the spinal cord, the brainstem, and the cerebral cortex. Delineation of the precise anatomic sites of action is difficult because many anesthetics diffusely inhibit electrical activity in the CNS. Anesthetics may produce specific components of the anesthetic state via actions at specific sites in the CNS. Inhalational anesthetics produce immobilization in response to a surgical incision (the end point used in determining MAC) by action on the spinal cord. Given that amnesia or unconsciousness cannot result from anesthetic actions in the spinal cord, different components of anesthesia must be produced at different sites in the CNS. Indeed, the sedative effects of pentobarbital and propofol (GABAergic anesthetics) are mediated by GABAA receptors in the tuberomammillary nucleus, and the sedative effects of the intravenous anesthetic dexmedetomidine (an a2 adrenergic receptor agonist) are produced via actions in the locus ceruleus, suggesting that the sedative actions of some anesthetics share the neuronal pathways involved in endogenous sleep. Inhalational anesthetics depress the excitability of thalamic neurons, pointing to the thalamus as a potential locus for the sedative effects of inhalational anesthetics, since blockade of thalamocortical communication would produce unconsciousness. Finally, both intravenous and inhalational anesthetics depress hippocampal neurotransmission, a probable locus for their amnestic effects.

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