Table 1 Glial signaling molecules and gliotransmitters affecting pathological pain. The table summarizes gliotransmitters released from spinal astrocytes that have important effects on pathological pain. The gliotransmitter-related mechanisms that strengthen or weaken pathological pain are described

TNFα

Excitatory transmission (+), Insertion of AMPA receptor (+), Presynaptic glutamate release (+), GABA receptor endocytosis (+)

Inhibition: development of neuropathic pain

[19,20,21,22]

IL-1β

Phosphorylation of NMDA receptor (+), Ca²⁺ entry (through NMDAR) (+), C-fiber-mediated long-term potentiation (+), Presynaptic glutamate release (+)

Inhibition: allodynia, Enhancement: hyperalgesia

[17, 21, 23,24,25]

thrombospondin (TSP)

Excitatory synaptogenesis (+), Excitatory synaptic transmission (+)

Inhibition: mechanical allodynia and thermal hyperalgesia

[26,27,28]

ATP

Excitability of nociceptor in DRG (+)

Inhibition: analgesic effect

[6], [17], [18], [30,31,32,33]

Adenosine

Synaptic transmission (-)

Enhancement: analgesic effect

[6], [18], [34]

D-serine

Potentiation of NMDA receptor (+), Increase of neuronal NOS (nNOS) activity (+), Nociceptive transmission (+), Chronic pain behavior (+)

Inhibition: mechanical allodynia

[35,36,37,38,39,40]

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 (-)

[41,42,43,44,45,46,47]