antinociception

Antinociception is the physiological and pharmacological process by which nociceptive signals—those that would normally provoke the perception of pain—are inhibited along the nervous system. It encompasses mechanisms that prevent the initiation, transmission, or perception of nociceptive information, and underlies the effects of many analgesic strategies. Antinociception can occur at peripheral sites, in the spinal cord, or in supraspinal brain regions, and may reduce both the sensory and affective components of pain.

Mechanisms include peripheral desensitization of nociceptors, reduced release of excitatory neurotransmitters, and modulation of ion channels. In the spinal cord, inhibitory interneurons in the dorsal horn can suppress nociceptive transmission via inhibitory neurotransmitters such as GABA and glycine, a concept linked to gate control theory. Descending pain-modulatory pathways from the brainstem, notably the periaqueductal gray and rostroventral medulla, release endogenous opioids, serotonin, and norepinephrine to dampen nociception. Endocannabinoids and other neuromodulators also contribute to antinociception.

Pharmacologically, opioids, nonsteroidal anti-inflammatory drugs, local anesthetics, gabapentinoids, and NMDA receptor antagonists can produce antinociception through different targets. Nonpharmacologic approaches, including cognitive modulation, physical therapy, and acupuncture, may also enhance antinociception or engage endogenous analgesic systems.

In clinical use, antinociception is a key objective of anesthesia and pain management. While commonly overlapping with analgesia, antinociception specifically refers to the suppression of nociceptive signaling, which can reduce pain perception under various conditions.