From: Role of spinal astrocytes through the perisynaptic astrocytic process in pathological pain
 | (+): strengthen |  | (-): weaken |  |
---|---|---|---|---|
Gliotransmitter | Proposed Functions | Roles in pathological pain | Reference | |
TNFα | Excitatory transmission (+), Insertion of AMPA receptor (+), Presynaptic glutamate release (+), GABA receptor endocytosis (+) | Inhibition: development of neuropathic pain | ||
IL-1β | Phosphorylation of NMDA receptor (+), Ca2+ entry (through NMDAR) (+), C-fiber-mediated long-term potentiation (+), Presynaptic glutamate release (+) | Inhibition: allodynia, Enhancement: hyperalgesia | ||
thrombospondin (TSP) | Excitatory synaptogenesis (+), Excitatory synaptic transmission (+) | Inhibition: mechanical allodynia and thermal hyperalgesia | ||
ATP | Excitability of nociceptor in DRG (+) | Inhibition: analgesic effect | ||
Adenosine | Synaptic transmission (-) | Enhancement: analgesic effect | ||
D-serine | Potentiation of NMDA receptor (+), Increase of neuronal NOS (nNOS)Â activity (+), Nociceptive transmission (+), Chronic pain behavior (+) | Inhibition: mechanical allodynia | ||
TRPA1/Ca2+-mediated gliotransmitters | Maintain the excitatory and inhibitory balance of neuronal activation (+) Astrocytic glutamate release (+), Maintain expression of GAT3(GABA transporter in astrocyte) (+), Modulate the astrocytic structural outgrowth or retraction of PAP. | Inhibition-TRPA1: acute and chronic pain (-) |