for several reasons. normally, the gap junctions between sgcs are used in order to redistribute potassium ions between adjacent cells. however, in coupling of sgcs, the number of gap junctions greatly increases. this may possibly be to deal with larger amounts of atp and glutamate, which eventually leads to increased recycling of the glutamate. the increased levels of glutamate lead to over excitation and an increase in nociception. expression of receptors and ion channels representation of a typical p2x receptor subunit associated with the plasma membrane. 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. herpes simplex herpes simplex virions. sensory ganglia have been associated with infections from viruses like herpes simplex, which can exist in a dormant state within the ganglia for decades after the primary infection. when the virus becomes reactivated, blisters on the skin and mucous membranes appear. during the latent stage of the virus, the viruses are rarely located in the sgcs within the sensory ganglia, but the sgcs may still play an important role within the disease. it has been proposed that sgcs act to create walls to prevent the spread of the virus from infected to uninfected neurons. if this wall of protection was to break down, then the infection could become more widespread. this property may be explained by looking at the location and arrangement of the sgcs, as they are centered on the neurons, allowing them to protect the neurons. it has also been proposed that sgcs may have a job in ridding the ganglia of the virus and in protecting and repairing the nervous system after the virus has left the dormant stage. research directions the majority of the information available on the subject of sgcs comes from research which was focused on the sensory neurons that the sgcs surround rather than the sgcs themselves. in the future, researchers plan to give more time and attention to the sgcs, which have many supportive and protective functions essential for life. neurotransmitter and hormone receptors on sgcs in situ rather than in culture will likely be explored and definitively characterized. changes in the receptors caused by various mutations and diseases will also be explored in order to determine the effect of these conditions. additionally, the mechanisms behind neuronal-sgc communication is essentially unidentified, though it is likely that the various receptors both the neurons and sgcs have are used for chemical signaling, perhaps with p2y. ca2+ and no and their effects must also be observed to gain further understanding of interactions between the two types of cells. finally, the possibility of an influence of sgcs on synaptic transmission within autonomic ganglia provides another direction for future research.