Acetylcholine receptors do not mediate the immobilization produced by inhaled anesthetics

Acetylcholine receptors transmit excitatory impulses, are broadly distributed throughout the central nervous system, and are particularly sensitive to the depressant effects of inhaled anesthetics. Thus these receptors are potential mediators of the immobility produced by inhaled anesthetics. We tested this potential in rats by giving intraperitoneal atropine, scopolamine, and mecamylamine to block muscarinic (atropine and scopolamine) and neuronal nicotinic (mecamylamine) acetylcholine receptors. Block with scopolamine (up to 100 mg/kg), atropine (10 mg/kg), mecamylamine (up to 4 mg/kg), or atropine (10 mg/kg) plus mecamylamine (up to 4 mg/kg) did not significantly decrease the isoflurane concentration required to suppress movement to noxious stimulation (minimum alveolar anesthetic concentration). We also gave atropine intrathecally, finding that the infusions that did not cause permanent paralysis produced slight or no decreases in the minimum alveolar anesthetic concentration. We conclude that acetylcholine receptors do not seem to play a role as mediators of immobilization by inhaled anesthetics.

Inhaled anesthetics produce two crucial effects: amnesia and immobility in the face of noxious stimulation. Block of muscarinic and neuronal nicotinic acetylcholine receptors in rats does not significantly decrease the isoflurane concentration required to suppress movement to stimulation. Thus, acetylcholine receptors do not seem to play a major role as mediators of the immobilization produced by inhaled anesthetics. Their capacity to mediate other effects of inhaled anesthetics (e.g., amnesia) remains to be tested.