Update on the neurophysiology of pain transmission and modulation: focus on the NMDA-receptor
by
Bennett GJ
Department of Neurology,
MCP Hahnemann University,
Philadelphia, Pennsylvania 19102-1192, USA.
J Pain Symptom Manage 2000 Jan; 19(1 Suppl):S2-6

ABSTRACT

Pain is detected by two different types of peripheral nociceptor neurons, C-fiber nociceptors with slowly conducting unmyelinated axons, and A-delta nociceptors with thinly myelinated axons. During inflammation, nociceptors become sensitized, discharge spontaneously, and produce ongoing pain. Prolonged firing of C-fiber nociceptors causes release of glutamate which acts on N-methyl-D-aspartate (NMDA) receptors in the spinal cord. Activation of NMDA receptors causes the spinal cord neuron to become more responsive to all of its inputs, resulting in central sensitization. NMDA-receptor antagonists, such as dextromethorphan, can suppress central sensitization in experimental animals. NMDA-receptor activation not only increases the cell's response to pain stimuli, it also decrease neuronal sensitivity to opioid receptor agonists. In addition to preventing central sensitization, co-administration of NMDA-receptor antagonists with an opioid may prevent tolerance to opioid analgesia.

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NMDA
Tilidine
Nociceptin
Buprenorphine
Opiated worms
NMDA antagonists
Fentanyl analogues
Fentanyl and ketamine
Remifentanil and alfentanil
Fentanyl: subjective effects
Pain and the NMDA receptor
NMDA antagonists for drug users
NMDA antagonists against morphine tolerance
NMDA antagonists, opioid receptors and tolerance
NMDA receptors and opiate-induced neural plasticity

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