[5] Many of these receptors and other ion channels have recently been implicated in health issues including chronic pain[6] and herpes simplex.

[8] Satellite glial cells are a type of glia found in the peripheral nervous system, specifically in sensory,[2] sympathetic, and parasympathetic ganglia.

On the other hand, mitochondria are found throughout the cytoplasm[10] along with the organelles involved in autophagy and other forms of catabolic degradation, such as lysosomes, lipofuscin granules, and peroxisomes.

[10] In some SGCs of the sensory ganglia researchers have seen a single cilium that extends outward from the cell surface near the nucleus and into the extracellular space of a deep indentation in the plasma membrane.

Many people liken SGCs to the astrocytes of the CNS because they share certain anatomical and physiological properties, such as the presence of neurotransmitter transporters and the expression of glutamine synthetase.

[2] These gap junctions have been identified through the use of electron microscopy and weight tracer markers, such as Lucifer yellow or neurobiotin.

The levels of GS are relatively low at rest, but they greatly increase if the neuron undergoes axonal damage.

This is based on the observation that SGCs almost completely envelop the neuron and can regulate the diffusion of molecules across the cell membrane.

[3] It has been previously shown that when fluorescent protein tracers are injected into the cervical ganglion in order to bypass the circulatory system, they are not found on the neuron surface.

An established mode of controlling the microenvironment in sensory ganglia is the uptake of substances by specialized transporters which carry neurotransmitters into cells when coupled with Na+ and Cl−.

Glial cells, including SGCs, have long been recognized for their roles in response to neuronal damage and injury.

[30] SGCs are present in the PNS in fewer numbers than other more well-known types of glial cells, like astrocytes, but have been determined to affect nociception because of some of their physiological and pharmacological properties.

Additionally, several research groups have found that SGC coupling increases after nerve damage, which has an effect on the perception of pain, likely for several reasons.

[21] 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.

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.

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.

In other cases, the receptors contribute to nociception through the modulation of the extracellular concentration of calcitonin gene related peptide (CGRP).

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.

[7] It has been proposed that SGCs act to create walls to prevent the spread of the virus from infected to uninfected neurons.

In the future, researchers plan to give more time and attention to the SGCs, which have many supportive and protective functions essential for life.

[2] Finally, the possibility of an influence of SGCs on synaptic transmission within autonomic ganglia provides another direction for future research.