t is apparent from the above discussion that N2O has multiple mechanisms of action that underlie its varied pharmacological properties. Current research indicates that the analgesic effect of N2O appears to be initiated by stimulated neuronal release of endogenous opioid peptides, with subsequent activation of opioid receptors and descending GABA and noradrenergic pathways that modulate nociceptive processing at the spinal level. The anxiolytic effect of N2O involves activation of the GABAA receptor through the benzodiazepine binding site, although whether N2O acts directly or indirectly upon the latter targets remains uncertain. The anxiolytic pathway that is stimulated includes a segment that involves a sequence of 3 key enzymes, NOS, soluble guanylyl cyclase, and PKG. The anesthetic effect of N2O appears to be caused by inhibition of NMDA glutamate receptors and removing its excitatory influence in the nervous system.