Various neuronal receptors present on SGCs have been named as participants in ATP-evoked pain signals, particularly the homomultimer P2X3 and the heteromultimer P2X2/3 purinoceptors.
In general, the P2X family of receptors responds to neuronally released ATP.
Each of the P2X subtypes are found in sensory neurons with the exception of the P2X7 receptor, which is selectively expressed by glial cells, including SGCs.
The receptor has been implicated in the release of interleukin IL-1β from macrophages or microglia and astrocytes.
The receptor likely has a part in the cascade of events that end with inflammation and neuropathic pain.
It has been discovered that this receptor has an antagonist in the form of A-317491, which, when present, has the ability to reduce both the evoked and unprompted firing of various classes of spinal neurons, as well as to inhibit release of IL-1β.
However, the outside influences of receptors P2X3 and P2Y1 are believed to complicate the interactions between P2X7 and its antagonist, making it a non-ideal target when using pharmacological strategy.

P2Y receptors are also found on both neurons and glial cells.
Their role is less clear than that of the P2X receptors, but it has been noted they have several conflicting functions.
In some cases, these receptors act as analgesics, as P2Y1 has the ability to inhibit the action of P2X3.
In other cases, the receptors contribute to nociception through the modulation of the extracellular concentration of calcitonin gene related peptide (CGRP).
These conflicting roles are being researched further so that they may serve as potential targets for the development of a variety of therapeutic drugs.

SGCs also express a specific type of channel, the Kir4.1 channel, which works to maintain the desired low extracellular K⁺ concentration in order to control hyperexcitability, which is known to cause migraines.
Additionally, extracellular K⁺ concentration has been found to be controlled by guanine nucleoside guanosine (Guo).
Guo, which may be involved in neuron-to-SGC communication and interaction in sensory ganglia, is also a potential target that could control the alterations of extracellular K⁺ concentration associated with chronic pain.
Various neuronal receptors present on SGCs have been named as participants in ATP-evoked pain signals, particularly the homomultimer P2X3 and the heteromultimer P2X2/3 purinoceptors. In general, the P2X family of receptors responds to neuronally released ATP. Each of the P2X subtypes are found in sensory neurons with the exception of the P2X7 receptor, which is selectively expressed by glial cells, including SGCs. The receptor has been implicated in the release of interleukin IL-1β from macrophages or microglia and astrocytes. The receptor likely has a part in the cascade of events that end with inflammation and neuropathic pain. It has been discovered that this receptor has an antagonist in the form of A-317491, which, when present, has the ability to reduce both the evoked and unprompted firing of various classes of spinal neurons, as well as to inhibit release of IL-1β. However, the outside influences of receptors P2X3 and P2Y1 are believed to complicate the interactions between P2X7 and its antagonist, making it a non-ideal target when using pharmacological strategy.
P2Y receptors are also found on both neurons and glial cells. Their role is less clear than that of the P2X receptors, but it has been noted they have several conflicting functions. In some cases, these receptors act as analgesics, as P2Y1 has the ability to inhibit the action of P2X3. In other cases, the receptors contribute to nociception through the modulation of the extracellular concentration of calcitonin gene related peptide (CGRP). These conflicting roles are being researched further so that they may serve as potential targets for the development of a variety of therapeutic drugs.
SGCs also express a specific type of channel, the Kir4.1 channel, which works to maintain the desired low extracellular K⁺ concentration in order to control hyperexcitability, which is known to cause migraines. Additionally, extracellular K⁺ concentration has been found to be controlled by guanine nucleoside guanosine (Guo). Guo, which may be involved in neuron-to-SGC communication and interaction in sensory ganglia, is also a potential target that could control the alterations of extracellular K⁺ concentration associated with chronic pain.
Satellite glial cell