Pain-activated microglia (immune cells) release pro-inflammatory cytokines, which activate glia {glial activation} and cause pain, but other glia types do not release cytokines in response to pain. Spinal glial activation affects nociceptive neurons at NMDA receptors.
Blocking glial activation with drugs blocks pathological pain. Blocking neuron pro-inflammatory-cytokine receptors with drugs does not affect normal pain responses but does decrease exaggerated pain responses. Intrathecal drugs {fluorocitrate} can inhibit glial metabolism. Acids {kynurenic acid} {2-amino-5-phosphonovaleric acid} (AP-5) can prevent such inhibition. Amines {6,7-dinitroquinoxaline-2,3-dione} (DNQX) {picrotoxin} and strychnine do not prevent such inhibition [Ma and Zhao, 2002] [Watkins et al., 2001].
Consciousness>Consciousness>Sense>Pain>Physiology
1-Consciousness-Sense-Pain-Physiology
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Date Modified: 2022.0224