Opioid agonists interact with receptors in the brain and in the spinal cord. The initial binding of opioids in the brain causes the release of the inhibitory neurotrans-mitter serotonin, which in turn induces inhibition of the dorsal horn neurons. Both the brain and the spinal cord are required for the production of a maximal analgesic effect following systemic administration of opioids, although analgesia can be elicited by spinal administration only. In the spinal cord, morphine inhibits the release of most nociceptive peptides. Morphine also affects descending noradrenergic pathways. Norepi-nephrine release in response to opioid administration results in an analgesic effect at the spinal level.

Opioids have profound effects upon the cerebrocor-tical regions that control the somatosensory and discriminative aspects of pain. Thus, the opioids suppress the perception of pain by eliminating or altering the emotional aspects of pain and inducing euphoria and sleep with higher doses. Patients become inattentive to the painful stimuli, less anxious, and more relaxed. Disruption of normal REM sleep occurs with opioid administration. In addition, opioids depress polysynaptic responses but can increase monosynaptic responses and lead to convulsant effects in high doses. In patients with chronic pain, the euphoric effect of opioids, mediated by the ^-receptor, is usually blunted. Some patients feel a dysphoric effect upon the administration of opioids, which is most likely mediated by the a-receptor.

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