Aging is associated with an increase in dye coupling and in gap junction number in satellite glial cells of murine dorsal root ganglia

Huang, Tian-Ying; Hanani, Menachem; Ledda, M.; Palo, S. De; Pannese, Ennio

doi:10.1016/j.neuroscience.2005.10.020

Cited by 38 publications

(24 citation statements)

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“…Such negative cross talk might represent a model for a new mechanism to inhibit afferent excitation to the spinal cord as GABA and ATP are coreleased within the dorsal horn (29). Dye coupling incidence between satellite glial cells associated with neurons has been reported in DRG (12). These results provide the possibility for functional coupling between satellite glial cells and neurons, i.e., GABA inhibition mediated via gap junctions, although the direct evidence supporting for this possibility is not sufficient.…”

Section: Discussionmentioning

confidence: 96%

Age-related changes in afferent responses in sensory neurons to mechanical stimulation of osteoblasts in coculture system

Asada

Okihara

Horiguchi

et al. 2012

American Journal of Physiology-Cell Physiology

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Asada K, Obata K, Horiguchi K, Takaki M. Age-related changes in afferent responses in sensory neurons to mechanical stimulation of osteoblasts in coculture system. Am J Physiol Cell Physiol 302: C757-C765, 2012. First published November 16, 2011 doi:10.1152/ajpcell.00362.2011.-Bone homeostasis is regulated by mechanical stimulation (MS). The sensory mechanism of bone tissue for MS remains unknown in the maintenance of bone homeostasis. We aimed to investigate the sensory mechanism from osteoblasts to sensory neurons in a coculture system by MS of osteoblasts. Primary sensory neurons isolated from dorsal root ganglia (DRG) of neonatal, juvenile, and adult mice and osteoblasts isolated from calvaria of neonatal mice were cocultured for 24 h. The responses in DRG neurons elicited by MS of osteoblasts with a glass micropipette were detected by increases in intracellular Ca 2ϩ concentration ([Ca 2ϩ ]i) with fluo 3-AM. In all developmental stages mice, [Ca 2ϩ ]i-increasing responses in osteoblasts were promptly elicited by MS. After a short delay, [Ca 2ϩ ]i-increasing responses were observed in neurites of DRG neurons. The osteoblastic response to second MS was largely attenuated by a stretch-activated Ca 2ϩ channel blocker, gadolinium. The increases of [Ca 2ϩ ]i in DRG neurons were abolished by a P2 receptor antagonist; suramin, a P2X receptor antagonist, pyridoxal-phosphate-6-azophenyl-2=,4=-disulfonate; and an ATP-hydrolyzing enzyme, apyrase. Satellite cells were found around DRG neurons in cocultured cells of only neonatal and juvenile mice. After satellite cells were removed, excessive abnormal responses to MS of osteoblasts were observed in neonatal neurites with unchanged osteoblast responses. The present study indicated that MS of bone tissue elicited afferent P2X receptor-mediated purinergic transmission to sensory neurons in all stages mice. This transmission is modulated by satellite cells, which may have protective actions on sensory neurons. dorsal root ganglia; calcium imaging; satellite cell; 5=-triphosphate; bone formation BONE HAS IMPORTANT ROLES IN supporting the body to maintain motor functions against the gravity and in storing minerals such as calcium and phosphate, resulting in an essential role player maintaining life. In the maintenance of bone homeostasis, mechanical stimulation (MS) to the bone plays critical roles. Mechanically unloading by prolonged bed rest, immobilization, or microgravity in space causes a marked loss of bone (28, 34). The atrophic changes in bone or heterotopic bone formations are observed in patients with neurological disorder (7, 10). It would be beneficial in treatments for the patients with neurological disorder and for aged patients with bone loss (24) to reveal the transduction mechanism of MS into bone homeostasis.Such studies (17) have been initiated from the molecular mechanism in bone underlying transduction of MS into a cellular response, although the benefits of MS have been well demonstrated in clinical settings. Activation of a variety of factors s...

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Section: Discussionmentioning

confidence: 96%

Age-related changes in afferent responses in sensory neurons to mechanical stimulation of osteoblasts in coculture system

Asada

Okihara

Horiguchi

et al. 2012

American Journal of Physiology-Cell Physiology

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“…It has been proposed that these SGCs separate each neuronal body from one another, precluding the establishment of any type of synapse (Pannese, 1981, 2010). Consistent with this proposal, numerous ultrastructural and dye coupling studies have failed to find morphological or functional evidence of GJCs between sensory neurons or between sensory neurons and SGCs (Stensaas and Fidone, 1977; Shinder et al, 1998; Sakuma et al, 2001; Zuriel and Devor, 2001; Chen et al, 2002; Hanani et al, 2002; Pannese et al, 2003; Huang et al, 2006). In contrast, SGCs are coupled electrically and metabolically through GJCs (Sakuma et al, 2001; Huang et al, 2006; Pannese, 2010).…”

Section: Introductionmentioning

confidence: 92%

“…Consistent with this proposal, numerous ultrastructural and dye coupling studies have failed to find morphological or functional evidence of GJCs between sensory neurons or between sensory neurons and SGCs (Stensaas and Fidone, 1977; Shinder et al, 1998; Sakuma et al, 2001; Zuriel and Devor, 2001; Chen et al, 2002; Hanani et al, 2002; Pannese et al, 2003; Huang et al, 2006). In contrast, SGCs are coupled electrically and metabolically through GJCs (Sakuma et al, 2001; Huang et al, 2006; Pannese, 2010). It is known that SGCs influence neuronal excitability (Hanani, 2005; Huang and Hanani, 2005) by modifying the extracellular K + concentration and the intracellular free Ca 2+ concentration (Pannese, 1981; Suadicani et al, 2009).…”

Section: Introductionmentioning

confidence: 92%

Opening of pannexin- and connexin-based channels increases the excitability of nodose ganglion sensory neurons

Retamal

Alcayaga

Verdugo

et al. 2014

Front. Cell. Neurosci.

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Satellite glial cells (SGCs) are the main glia in sensory ganglia. They surround neuronal bodies and form a cap that prevents the formation of chemical or electrical synapses between neighboring neurons. SGCs have been suggested to establish bidirectional paracrine communication with sensory neurons. However, the molecular mechanism involved in this cellular communication is unknown. In the central nervous system (CNS), astrocytes present connexin43 (Cx43) hemichannels and pannexin1 (Panx1) channels, and the opening of these channels allows the release of signal molecules, such as ATP and glutamate. We propose that these channels could play a role in glia-neuron communication in sensory ganglia. Therefore, we studied the expression and function of Cx43 and Panx1 in rat and mouse nodose-petrosal-jugular complexes (NPJcs) using confocal immunofluorescence, molecular and electrophysiological techniques. Cx43 and Panx1 were detected in SGCs and in sensory neurons, respectively. In the rat and mouse, the electrical activity of vagal nerve increased significantly after nodose neurons were exposed to a Ca2+/Mg2+-free solution, a condition that increases the open probability of Cx hemichannels. This response was partially mimicked by a cell-permeable peptide corresponding to the last 10 amino acids of Cx43 (TAT-Cx43CT). Enhanced neuronal activity was reduced by Cx hemichannel, Panx1 channel and P2X7 receptor blockers. Moreover, the role of Panx1 was confirmed in NPJc, because in those from Panx1 knockout mice showed a reduced increase of neuronal activity induced by Ca2+/Mg2+-free extracellular conditions. The data suggest that Cx hemichannels and Panx channels serve as paracrine communication pathways between SGCs and neurons by modulating the excitability of sensory neurons.

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“…This is in contrast to the CNS where individual astrocytes are in contact with multiple neurons [24]. While the function of the satellite glia remains to be fully defined, both sympathetic and sensory satellite glia share several cellular and molecular features with astrocytes, including expression of neurotransmitter receptors and the formation of a glia network via gap junctions [25]. Satellite glia injury responses are characterized by changes in expression profiles, including an up-regulation of the activation marker glial fibrillary acidic protein (GFAP) [26].…”

Section: Introductionmentioning

confidence: 99%

Satellite glial cells modulate cholinergic transmission between sympathetic neurons

Enes

Sona

Gerard

et al. 2019

Preprint

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Satellite glial regulation of sympathetic activity" 15 16 17 18 40 Introduction 41 Glial cells, once thought of as neuron support cells, are now recognized as 42 active players in the formation and function of normal brain circuitry [1, 2]. 43 Astrocytes, the most abundant glial cell type in the brain, regulate many properties 44 of neuronal circuits such as neuronal excitability, synaptic transmission and 45 plasticity [3-5]. Their role at central nervous system (CNS) synapses has been the 46 focus of a number of studies in the past two decades, showing that astrocytes control 47 4 61 under pathological conditions such as hypertension and chronic heart disease [20, 62 21]. Sympathetic tone is initially set by neurons present in the brain and spinal cord 63 [22], with the sympathetic ganglionic neurons acting as the final regulatory element 64 determining the output of the sympathetic circuit. 65 A striking anatomical feature of the sympathetic ganglion is the presence of 66 satellite glia that form an envelope around individual ganglionic neuronal somata 67 and cover synapses [23]. This is in contrast to the CNS where individual astrocytes 68 are in contact with multiple neurons [24]. While the function of the satellite glia 69 remains to be fully defined, both sympathetic and sensory satellite glia share several 70 cellular and molecular features with astrocytes, including expression of 71 neurotransmitter receptors and the formation of a glia network via gap junctions 72 [25]. Satellite glia injury responses are characterized by changes in expression 73 profiles, including an up-regulation of the activation marker glial fibrillary acidic 74 protein (GFAP) [26]. These findings point to a possible effect in disease progression 75 and suggest that satellite glia play roles in both normal function and disease in the 76 peripheral nervous system. 77 Recent studies using genetic manipulations of sympathetic satellite glia have 78 implicated these cells in the regulation of target organ function by demonstrating 79 that selective activation of Gq-GPCR (G protein-coupled receptor) signaling in 80 peripheral glia leads to the modulation of cardiac properties in adult mice [27, 28]. 81 These effects are mediated through postganglionic sympathetic innervation of the 82 heart raising the possibility that activated glia influence the active properties of 157 in 4% paraformaldehyde (PFA) and then cryo-protected by incubating them in 30%

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Aging is associated with an increase in dye coupling and in gap junction number in satellite glial cells of murine dorsal root ganglia

Cited by 38 publications

References 36 publications

Age-related changes in afferent responses in sensory neurons to mechanical stimulation of osteoblasts in coculture system

Age-related changes in afferent responses in sensory neurons to mechanical stimulation of osteoblasts in coculture system

Opening of pannexin- and connexin-based channels increases the excitability of nodose ganglion sensory neurons

Satellite glial cells modulate cholinergic transmission between sympathetic neurons

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