Expression and contribution of satellite glial cells purinoceptors to pain transmission in sensory ganglia: an update

2010 ◽  
Vol 6 (1) ◽  
pp. 31-42 ◽  
Author(s):  
Giovanni Villa ◽  
Marta Fumagalli ◽  
Claudia Verderio ◽  
Maria P. Abbracchio ◽  
Stefania Ceruti
Keyword(s):  
Glial Cells ◽  
Pain Treatment ◽  
Purinergic Signaling ◽  
Original Data ◽  
P2y Receptors ◽  
Receptor Expression ◽  
Sensory Ganglia ◽  
Satellite Glial Cells ◽  
Pain Transmission

The role of adenosine-5′-triphosphate (ATP) and of the ligand-gated P2X3receptor in neuronal dorsal root ganglia (DRG) pain transmission is relatively well established. Much less is known about the purinergic system in trigeminal ganglia (TG), which are involved in certain types of untreatable neuropathic and inflammatory pain, as well as in migraine. Emerging data suggest that purinergic metabotropic P2Y receptors on both neurons and satellite glial cells (SGCs) may also participate in both physiological and pathological pain development. Here, we provide an updated literature review on the role of purinergic signaling in sensory ganglia, with special emphasis on P2Y receptors on SGCs. We also provide new original data showing a time-dependent downregulation of P2Y2and P2Y4receptor expression and function in purified SGCs cultures from TG, in comparison with primary mixed neuron–SGCs cultures. These data highlight the importance of the neuron–glia cross-talk in determining the SGCs phenotype. Finally, we show that, in mixed TG cultures, both adenine and guanosine induce intracellular calcium transients in neurons but not in SGCs, suggesting that also these purinergic-related molecules can participate in pain signaling. These findings may have relevant implications for the development of new therapeutic strategies for chronic pain treatment.

Aquaporin 4 expression on trigeminal satellite glial cells under normal and inflammatory conditions

2017 ◽  
Vol 16 (1) ◽  
pp. 183-184
Author(s):  
D. Riccio ◽  
G. Magni ◽  
S. Ceruti ◽  
L. Arendt-Nielsen ◽  
P. Gazerani
Keyword(s):  
Glial Cells ◽  
Trigeminal Ganglia ◽  
Sensory Ganglia ◽  
Satellite Glial Cells ◽  
Pain Model ◽  
Aqp4 Expression ◽  
Inflammatory Conditions ◽  
Trigeminal Neurons ◽  
Deficient Mice

AbstractAimsLimited information is currently available for the expression and role of Aquaporin 4 (AQP4) (AQ4) in the peripheral nervous system (PNS). It has been demonstrated that AQP4 is expressed in sensory ganglia. Immunohistochemistry has revealed that satellite glial cells (SGCs) surrounding the cell bodies of the primary afferent sensory neurons in these sensory ganglia exclusively express AQP4 at a considerably lower level than what is seen in astrocytes. The pathophysiological relevance of AQP4 in peripheral nociception; however, remains unclear. Hence, this study aimed at investigating AQP4 expression in trigeminal neurons and SGCs under normal and inflammatory conditions relevant to craniofacial pain conditions.MethodsRat trigeminal ganglia (TG) were isolated from adult male Sprague-Dawley rats subjected to a model of trigeminal inflammation evoked by unilateral complete Freund’s adjuvant (CFA) injection in temporomandibular joint. Immunohistochemistry was performed on TG sections of CFA-treated animals. NeuN and GS markers were used for identification of neurons and SGCs, respectively. AQP4 expression was investigated in both ipsilateral and contralateral TG sections. The study protocol was approved by the local ethics committee.ResultsCo-localization of NeuN-AQP4 and GS-AQP4 were identified in both ipsi and contralateral trigeminal ganglia of the CFA-treated rats. However, we did not detect any difference between the ipsi- and contralateral side in terms of alteration in AQP4 receptor expression.ConclusionsAQP4 was expressed both on trigeminal neurons and SGCs and CFA did not cause a remarkable change in AQP4 expression, when ipsilateral and contralateral TG of the test animals was compared. Previously, it has been shown that in a neuropathic pain model no difference is detectable between wild type and AQP4-deficient mice, for mechanical and thermal perception; however, in formalin pain model AQP4-deficient mice have higher thermal pain thresholds. Further investigation is required to clarify role of AQP4 in pain.

scholarly journals Satellite glial cells in sensory ganglia express functional transient receptor potential ankyrin 1 that is sensitized in neuropathic and inflammatory pain

2020 ◽  
Vol 16 ◽  
pp. 174480692092542 ◽  
Author(s):  
Seung Min Shin ◽  
Brandon Itson-Zoske ◽  
Yongsong Cai ◽  
Chensheng Qiu ◽  
Bin Pan ◽  
...  
Keyword(s):  
Neuropathic Pain ◽  
Nerve Injury ◽  
Glial Cells ◽  
Transient Receptor Potential ◽  
Receptor Potential ◽  
Allyl Isothiocyanate ◽  
Sensory Ganglia ◽  
Satellite Glial Cells ◽  
Intracellular Ca ◽  
Transient Receptor

Transient receptor potential ankyrin 1 (TRPA1) is well documented as an important molecule in pain hypersensitivity following inflammation and nerve injury and in many other cellular biological processes. Here, we show that TRPA1 is expressed not only by sensory neurons of the dorsal root ganglia (DRG) but also in their adjacent satellite glial cells (SGCs), as well as nonmyelinating Schwann cells. TRPA1 immunoreactivity is also detected in various cutaneous structures of sensory neuronal terminals, including small and large caliber cutaneous sensory fibers and endings. The SGC-expressed TRPA1 is functional. Like DRG neurons, dissociated SGCs exhibit a robust response to the TRPA1-selective agonist allyl isothiocyanate (AITC) by an increase of intracellular Ca2+ concentration ([Ca2+]i). These responses are abolished by the TRPA1 antagonist HC030031 and are absent in SGCs and neurons from global TRPA1 null mice. SGCs and neurons harvested from DRG proximal to painful tissue inflammation induced by plantar injection of complete Freund’s adjuvant show greater AITC-evoked elevation of [Ca2+]i and slower recovery compared to sham controls. Similar TRPA1 sensitization occurs in both SGCs and neurons during neuropathic pain induced by spared nerve injury. Together, these results show that functional TRPA1 is expressed by sensory ganglia SGCs, and TRPA1 function in SGCs is enhanced after both peripheral inflammation and nerve injury, and suggest that TRPA1 in SGCs may contribute to inflammatory and neuropathic pain.

Purinergic signaling between neurons and satellite glial cells of mouse dorsal root ganglia modulates neuronal excitability in vivo

Pain ◽  
2021 ◽  
Vol Publish Ahead of Print ◽  
Author(s):  
Zhiyong Chen ◽  
Qian Huang ◽  
Xiaodan Song ◽  
Neil C. Ford ◽  
Chi Zhang ◽  
...  
Keyword(s):  
Glial Cells ◽  
Dorsal Root Ganglia ◽  
Dorsal Root ◽  
Neuronal Excitability ◽  
Purinergic Signaling ◽  
Satellite Glial Cells

scholarly journals Purinergic signaling and the functioning of the nervous system cells

2015 ◽  
Vol 20 (5) ◽  
Author(s):  
Kamila Puchałowicz ◽  
Irena Baranowska-Bosiacka ◽  
Violetta Dziedziejko ◽  
Dariusz Chlubek
Keyword(s):  
Nervous System ◽  
Glial Cells ◽  
Purinergic Signaling ◽  
Physiological State ◽  
P2y Receptors ◽  
Mechanisms Of Action ◽  
Synaptic Activity ◽  
Extracellular Nucleotides ◽  
Synaptic Connections ◽  
P2x And P2y Receptors

AbstractPurinergic signaling in the nervous system has been the focus of a considerable number of studies since the 1970s. The P2X and P2Y receptors are involved in the initiation of purinergic signaling. They are very abundant in the central and peripheral nervous systems, where they are expressed on the surface of neurons and glial cells - microglia, astrocytes, oligodendrocytes and Schwann cells and the precursors of the latter two. Their ligands - extracellular nucleotides - are released in the physiological state by astrocytes and neurons forming synaptic connections, and are essential for the proper functioning of nervous system cells. Purinergic signaling plays a crucial role in neuromodulation, neurotransmission, myelination in the CNS and PNS, intercellular communication, the regulation of ramified microglia activity, the induction of the response to damaging agents, the modulation of synaptic activity and other glial cells by astrocytes, and the induction of astrogliosis. Understanding these mechanisms and the fact that P2 receptors and their ligands are involved in the pathogenesis of diseases of the nervous system may help in the design of drugs with different and more effective mechanisms of action.

Quiescent satellite glial cells of the adult trigeminal ganglion

Open Medicine ◽  
2014 ◽  
Vol 9 (3) ◽  
pp. 500-504 ◽  
Author(s):  
Mugurel Rusu ◽  
Valentina Mănoiu ◽  
Nicolae Mirancea ◽  
Gheorghe Nini
Keyword(s):  
Electron Microscopy ◽  
Glial Cells ◽  
Trigeminal Ganglion ◽  
Membrane Trafficking ◽  
Animal Species ◽  
Trigeminal Ganglia ◽  
Sensory Ganglia ◽  
Satellite Glial Cells ◽  
Transmission Electron ◽  
Immune Phenotypes

AbstractSensory ganglia comprise functional units built up by neurons and satellite glial cells (SGCs). In animal species there was proven the presence of neuronoglial progenitor cells in adult samples. Such neural crest-derived progenitors were found in immunohistochemistry (IHC). These findings were not previously documented in transmission electron microscopy (TEM). It was thus aimed to assess in TEM if cells of the human adult trigeminal ganglion indeed have ultrastructural features to qualify for a progenitor, or quiescent phenotype. Trigeminal ganglia were obtained from fifteen adult donor cadavers. In TEM, cells with heterochromatic nuclei, a pancytoplasmic content of free ribosomes, few perinuclear mitochondria, poor developed endoplasmic reticulum, lack of Golgi complexes and membrane trafficking specializations, were found included in the neuronal envelopes built-up by SGCs. The ultrastructural pattern was strongly suggestive for these cells being quiescent progenitors. However, further experiments should correlate the morphologic and immune phenotypes of such cells.

scholarly journals The Impact of Purinergic System Enzymes on Noncommunicable, Neurological, and Degenerative Diseases

2018 ◽  
Vol 2018 ◽  
pp. 1-21 ◽  
Author(s):  
Margarete Dulce Bagatini ◽  
Alessandra Antunes dos Santos ◽  
Andréia Machado Cardoso ◽  
Aline Mânica ◽  
Cristina Ruedell Reschke ◽  
...  
Keyword(s):  
Molecular Mechanisms ◽  
Purinergic Signaling ◽  
P2y Receptors ◽  
Degenerative Diseases ◽  
Limited Effectiveness ◽  
Central Nervous Systems ◽  
Health And Disease ◽  
The Impact

Evidences show that purinergic signaling is involved in processes associated with health and disease, including noncommunicable, neurological, and degenerative diseases. These diseases strike from children to elderly and are generally characterized by progressive deterioration of cells, eventually leading to tissue or organ degeneration. These pathological conditions can be associated with disturbance in the signaling mediated by nucleotides and nucleosides of adenine, in expression or activity of extracellular ectonucleotidases and in activation of P2X and P2Y receptors. Among the best known of these diseases are atherosclerosis, hypertension, cancer, epilepsy, Alzheimer’s disease (AD), Parkinson’s disease (PD), and multiple sclerosis (MS). The currently available treatments present limited effectiveness and are mostly palliative. This review aims to present the role of purinergic signaling highlighting the ectonucleotidases E-NTPDase, E-NPP, E-5′-nucleotidase, and adenosine deaminase in noncommunicable, neurological, and degenerative diseases associated with the cardiovascular and central nervous systems and cancer. In conclusion, changes in the activity of ectonucleotidases were verified in all reviewed diseases. Although the role of ectonucleotidases still remains to be further investigated, evidences reviewed here can contribute to a better understanding of the molecular mechanisms of highly complex diseases, which majorly impact on patients’ quality of life.

How do neurons in sensory ganglia communicate with satellite glial cells?

2021 ◽  
Vol 1760 ◽  
pp. 147384
Author(s):  
Rachel Feldman-Goriachnik ◽  
Menachem Hanani
Keyword(s):  
Glial Cells ◽  
Sensory Ganglia ◽  
Satellite Glial Cells

scholarly journals Mechanisms of ATP release in pain: role of pannexin and connexin channels

2021 ◽  
Author(s):  
Manuel F. Muñoz ◽  
Theanne N. Griffith ◽  
Jorge E. Contreras
Keyword(s):  
Purinergic Receptors ◽  
Pain Treatment ◽  
Purinergic Signaling ◽  
Atp Release ◽  
Current Evidence ◽  
Pain Processing ◽  
Potential Threat ◽  
Acute Response ◽  
Outstanding Question

AbstractPain is a physiological response to bodily damage and serves as a warning of potential threat. Pain can also transform from an acute response to noxious stimuli to a chronic condition with notable emotional and psychological components that requires treatment. Indeed, the management of chronic pain is currently an important unmet societal need. Several reports have implicated the release of the neurotransmitter adenosine triphosphate (ATP) and subsequent activation of purinergic receptors in distinct pain etiologies. Purinergic receptors are broadly expressed in peripheral neurons and the spinal cord; thus, purinergic signaling in sensory neurons or in spinal circuits may be critical for pain processing. Nevertheless, an outstanding question remains: what are the mechanisms of ATP release that initiate nociceptive signaling? Connexin and pannexin channels are established conduits of ATP release and have been suggested to play important roles in a variety of pathologies, including several models of pain. As such, these large-pore channels represent a new and exciting putative pharmacological target for pain treatment. Herein, we will review the current evidence for a role of connexin and pannexin channels in ATP release during nociceptive signaling, such as neuropathic and inflammatory pain. Collectively, these studies provide compelling evidence for an important role of connexins and pannexins in pain processing.

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