GABA-mediated modulation of ATP-induced intracellular calcium responses in nodose ganglion neurons of the rat

Yokoyama, Takuya; Fukuzumi, Shou; Hayashi, Hitomi; Nakamuta, Nobuaki; Yamamoto, Yoshio

doi:10.1016/j.neulet.2014.10.008

Cited by 6 publications

(8 citation statements)

References 20 publications

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“…There is evidence for orexin receptors in SGCs in rat and human NG (Burdyga et al, 2003 ) and for BDNF receptors on SGCs in NG of rats (Wetmore and Olson, 1995 ). A calcium imaging study has shown that SGCs in rat NG are sensitive to glutamate and to ATP (via P2YR) and can release GABA (Shoji et al, 2010 ; Yokoyama et al, 2015 ). These authors claimed that GABA release from SGCs onto nodose neurons can inhibit neuronal activity.…”

Section: Sgcs In Nodose Gangliamentioning

confidence: 99%

Role of satellite glial cells in gastrointestinal pain

Hanani

2015

Front. Cell. Neurosci.

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Gastrointestinal (GI) pain is a common clinical problem, for which effective therapy is quite limited. Sensations from the GI tract, including pain, are mediated largely by neurons in the dorsal root ganglia (DRG), and to a smaller extent by vagal afferents emerging from neurons in the nodose/jugular ganglia. Neurons in rodent DRG become hyperexcitable in models of GI pain (e.g., gastric or colonic inflammation), and can serve as a source for chronic pain. Glial cells are another element in the pain signaling pathways, and there is evidence that spinal glial cells (microglia and astrocytes) undergo activation (gliosis) in various pain models and contribute to pain. Recently it was found that satellite glial cells (SGCs), the main type of glial cells in sensory ganglia, might also contribute to chronic pain in rodent models. Most of that work focused on somatic pain, but in several studies GI pain was also investigated, and these are discussed in the present review. We have shown that colonic inflammation induced by dinitrobenzene sulfonic acid (DNBS) in mice leads to the activation of SGCs in DRG and increases gap junction-mediated coupling among these cells. This coupling appears to contribute to the hyperexcitability of DRG neurons that innervate the colon. Blocking gap junctions (GJ) in vitro reduced neuronal hyperexcitability induced by inflammation, suggesting that glial GJ participate in SGC-neuron interactions. Moreover, blocking GJ by carbenoxolone and other agents reduces pain behavior. Similar changes in SGCs were also found in the mouse nodose ganglia (NG), which provide sensory innervation to most of the GI tract. Following systemic inflammation, SGCs in these ganglia were activated, and displayed augmented coupling and greater sensitivity to the pain mediator ATP. The contribution of these changes to visceral pain remains to be determined. These results indicate that although visceral pain is unique, it shares basic mechanisms with somatic pain, suggesting that therapeutic approaches to both pain types may be similar. Future research in this field should include additional types of GI injury and also other types of visceral pain.

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Section: Sgcs In Nodose Gangliamentioning

confidence: 99%

Role of satellite glial cells in gastrointestinal pain

Hanani

2015

Front. Cell. Neurosci.

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“…However, we did not analyse the structural connections between GABA A Rs and P2X7Rs in the SCG, and these two receptors may work separately. According to previous reports, 35,36 we hypothesize ( Figure 6) that GABA A Rs and P2X7Rs interact inside the cell membrane to exert an inhibitory function in SCG sympathetic neurons, but the mechanism requires further investigation.…”

Section: Gabaergic Signalling System and Arrhythmiasmentioning

confidence: 59%

“…Thus, we concluded that GABA A Rβ 2 was the major target. 35 A molecular study demonstrated an interaction of GABA A Rs and P2XRs in mouse spinal cord neurons and that GABA A R distribution and dynamics were modulated by P2XRs. Thus, we could not exclude the possibility that regional differences in GABA inhibition within the SCG were because of GABA A Rα4 subunit distribution or other subunits in the SCG.…”

Section: Gaba Inhibition In the Rat Scgmentioning

confidence: 99%

“…Recent articles have provided clues showing that GABA may reduce ATP-induced intracellular Ca 2+ elevation through P2XRs in rat nodose ganglion neurons. 35 A molecular study demonstrated an interaction of GABA A Rs and P2XRs in mouse spinal cord neurons and that GABA A R distribution and dynamics were modulated by P2XRs. 36 Because SCG neurons were positive for both P2X7Rs and GABA A Rs, we examined changes in intracellular Ca 2+ levels using two receptor agonists, ATP and muscimol.…”

Section: Gaba Inhibition In the Rat Scgmentioning

confidence: 99%

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A novel sympathetic neuronal GABAergic signalling system regulates NE release to prevent ventricular arrhythmias after acute myocardial infarction

Shi

Yin

et al. 2019

Acta Physiologica

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Aim:Overactivation of the sympathetic nerve may lead to severe ventricular arrhythmias (VAs) after myocardial infarction (MI). Thus, targeting sympathetic nerve activity is an effective strategy to prevent VAs clinically. The superior cervical ganglion (SCG), the extracardiac sympathetic ganglion innervating cardiac muscles, has been found to have a GABAergic signalling system, the physiological significance of which is obscure. We aimed to explore the functional significance of SCG post MI and whether the GABAergic signal system is involved in the process. Methods: Adult male Sprague-Dawley rats were divided into seven different groups. Rats in the MI groups underwent ligation of the left anterior descending coronary artery. All animals were used for electrophysiological testing, renal sympathetic nerve activity (RSNA) testing, and ELISA. Primary SCG sympathetic neurons were used for the in vitro study. Results: The GABA A receptor agonist muscimol significantly decreased the ATPinduced increase in intracellular Ca 2+ (P < 0.05). GABA treatment in MI rats significantly attenuated the level of serum and cardiac norepinephrine (NE; P < 0.05).Sympathetic activity and inducible VAs were also lower in MI + GABA rats than in MI rats (P < 0.05). Knockdown of the GABA A Rs β 2 subunit (GABA A Rβ 2 ) in the SCG of MI rats increased the NE levels in serum and cardiac tissue, RSNA and inducible VAs compared with vehicle shRNA (P < 0.05). Conclusion: The GABAergic signalling system is functionally expressed in SCG sympathetic neurons, and activation of this system suppresses sympathetic activity, thereby facilitating cardiac protection and making it a potential target to alleviate VAs. K E Y W O R D Sarrhythmias, GABA, myocardial infarction, superior cervical ganglia, sympathetic nerve activity 2 of 14 | SHI et al.

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“…Previous electrophysiological and Ca 2+ imaging studies have shown that the fast excitatory effects of ATP on NG neurons were mediated by pharmacologically identified P2X2, P2X3, and heteromeric P2X2/3 receptors [26]. In addition, P2Y receptors play an important role in the mobilization of [Ca 2+ ] i from intracellular stores and can be activated by released ATP [15,27,28]. Satellite glial cells are the predominant glial cell controlling the neuronal microenvironment of sensory ganglia, including the NG (see [29]).…”

Section: Discussionmentioning

confidence: 99%

Purinergic receptor expression and function in rat vagal sensory neurons innervating the stomach

Blanke

Stella

Ruiz‐Velasco

et al. 2019

Neuroscience Letters

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The nodose ganglion (NG) is the main parasympathetic ganglion conveying sensory signals to the CNS from numerous visceral organs including digestive signals such as gastric distension or the release the gastrointestinal peptides. The response characteristics of NG neurons to ATP and ADP and pharmacological interrogation of purinergic receptor subtypes have been previously investigated but often in NG cells of undetermined visceral origin. In this study, we confirmed the presence of P2X3 and P2Y1 receptors and characterized P2X and P2Y responses in gastric-innervating NG neurons. Application of ATP-evoked large inward currents and cytosolic Ca2+ increases in gastric-innervating NG neurons. Despite the expression of P2Y1 receptors, ADP elicited only minor modulation of voltage-gated Ca2+ channels. Considering the sensitivity of NG neurons to comorbidities associated with disease or neural injury, purinergic modulation of gastric NG neurons in disease- or injury-states is worthy of further investigation.

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GABA-mediated modulation of ATP-induced intracellular calcium responses in nodose ganglion neurons of the rat

Cited by 6 publications

References 20 publications

Role of satellite glial cells in gastrointestinal pain

Role of satellite glial cells in gastrointestinal pain

A novel sympathetic neuronal GABAergic signalling system regulates NE release to prevent ventricular arrhythmias after acute myocardial infarction

Purinergic receptor expression and function in rat vagal sensory neurons innervating the stomach

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