ATP as a Co‐Transmitter with Noradrenaline in Sympathetic Nerves—Function and Fate

Kennedy, Charles; McLaren, Gerald J.; Westfall, Timothy D.; Sneddon, Peter

doi:10.1002/9780470514900.ch13

Cited by 16 publications

(12 citation statements)

References 32 publications

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“…ATP seems to be the most enigmatic signalling molecule, since it was reported to transmit and essentially modulate the cross-talk between neuronalneuronal and neuronal-glial elements in high brain regions. It was found recently that ATP is co-released with other transmitters in several brain structures [26][27][28]. It is well known that high-frequency stimulation leads to ATP release in the hippocampus [29].…”

Section: Discussionmentioning

confidence: 99%

Influence of purinergic modulators on eEPSCs in rat CA3 hippocampal neurons: Contribution of ionotropic ATP receptors

2008

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ATP is considered to impact on fast synaptic transmission in several regions of the CNS, including the CA1 and CA3 areas of the hippocampus. The existing paradigm suggests that ATP induces synaptic responses in CA3 pyramidal cells, and a fast ATP-mediated component is observed in cultured hippocampal slices mainly under conditions of a synchronous discharge from multiple presynaptic inputs. We confirmed the existence of a fast ATP-mediated component within electrically evoked EPSCs (eEPSCs) in CA3 neurons of acute slices of the rat hippocampus using a whole-cell patch-clamp recording mode. In approximately 50% of the examined cells, eEPSCs were not completely inhibited by co-applied glutamate receptor antagonists, NBQX (50 µM) and D-APV (25 µM). The residual current was sensitive to ionotropic P2X receptor antagonists, such as suramin (25 µM) and NF023 (2 µM). Known purinergic receptor modulators, ivermectin (10 µM) and PPADS (10 µM), practically did not affect EPSCs, whereas a nonhydrolyzable ATP analog, ATPγS (100 µM), slightly decreased the EPSC amplitude. Moreover, ATPγS (100 µM) at a holding potential of -70 mV generated a slow inward current in most recorded neurons, which was insensitive to glutamate receptor antagonists. This fact is indicative of the ionotropic P2X receptor activation.

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Section: Discussionmentioning

confidence: 99%

Influence of purinergic modulators on eEPSCs in rat CA3 hippocampal neurons: Contribution of ionotropic ATP receptors

2008

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“…released by astrocytes through vesicle shedding [12,13]. The physiological release of uracil nucleotides is still a matter of debate.…”

Section: Purines and Pyrimidinesmentioning

confidence: 99%

Astrocytes in the damaged brain: Molecular and cellular insights into their reactive response and healing potential

Buffo

Rolando

Ceruti

2010

Biochemical Pharmacology

288

260

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This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. A c c e p t e d M a n u s c r i p t 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30 31 32 33 34 35 36 37 38 39 40 41 42 43 44 45 46 47 48 49 50 51 52 53 54 55 56 57 58 59 60 61 62 63 64 65 2 Running title: Beneficial and detrimental outcomes of astrogliosis after central nervous system injury. Abbreviations:Ado, adenosine; AMPA, alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionate; AP1, activator protein1; AQP, acquaporin; BBB, blood-brain barrier; BDNF, brain-derived growth factor; bFGF, basic fibroblast growth factor; bHLH, basic helix loop helix; BMP, bone morphogenetic protein; CNS, central nervous system; CNTF, ciliary neurotrophic factor;COX-2, cyclooxigenase-2; CREB, cAMP response element binding; CSPGs, chondroitinsulphate proteoglycans; ERK, extracellular signal-regulated kinase; EGF, epidermal growth factor; Eph4A, ephrin 4A; Epo, erythropoietin; ET1, Endothelin 1; ET-R, endothelin receptor; GABA, gamma-aminobutyric acid; GDNF, glial cell-line derived neurotropic factor; GF, growth factor; GFAP, glial fibrillary acidic protein; GLAST, glutamate aspartate transporter; GLT1, glutamate transporter 1; GS, glutamine synthase; IFN , interferon-beta; IFNγ, interferon gamma; IGF1, insulin growth factor1; IL1β, interleukin 1 beta; IL2, interleukin 2; IL6, interleukin 6; IL10, interleukin 10; JAK, Janus protein tyrosine kinases; Lcn2, Lipocalin 2; MAPK, mitogen-activated protein kinase; MMP, matrix metalloprotease; mTOR, mammalian target of rapamycin; NFAT, nuclear factor of activated T cell; NFkB, nuclear factor kappa B; NGF, nerve growth factor; NT3, neurotrophin 3; p38MAPK, p38 mitogen-activated protein kinase; PTEN, phosphatase and tensin homolog; SOCS, suppressor of cytokine signaling; SOD, superoxide dismutase; STAT, signal transducers and activators of transcription; TGFα, transforming growth factor alpha;TGFβ, transforming growth factor beta; TNFα, tumor necrosis factor alpha; VCAM1, vascular cell adhesion molecule-1; VEGF, vascular endothelial growth factor. Page 4 of 63A c c e p t e d M a n u s c r i p t 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30 31 32 33 34 35 36 37 38 39 40 41 42 43 44 45 46 47 48 49 50 51 52 53 54 55 56 57 58 59 60 61 62 63 64 A c c e p t e d M a n u s c r i p t 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30 31 32 33 34 35 36 37 38 39 40 41 42 43 4...

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“…To avoid such complications and to prolong the effects of released ATP, investigators frequently use inhibitors of ATP hydrolysis (7, 8, 9, 10, 11, 12). 6-N,N-diethyl-beta, gamma-dibromomethylene-D-ATP (ARL-67156, formerly known as FPL 67156) (13) is the first inhibitor of ectoATPase introduced for research (14) and is frequently utilized to inhibit ATP hydrolysis in tissue preparations. The majority of studies however do not validate the inhibitory action of ARL-67156 on the degradation of ATP and other purines although it is acknowledged that same enzymes could be involved in the degradation not only of ATP but also of ADP (15).…”

Section: Introductionmentioning

confidence: 99%

A commonly used ecto‐ATPase inhibitor, ARL‐67156, blocks degradation of ADP more than the degradation of ATP in murine colon

Durnin

Moreland

Lees

et al. 2016

Neurogastroenterology Motil

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Background Adenosine 5’-triphosphate (ATP) is released extracellularly as a neurotransmitter and an autocrine or paracrine mediator in numerous systems, including the gastrointestinal tract. It is rapidly degraded to active and inactive metabolites by membrane-bound enzymes. Investigators frequently use inhibitors of ATP hydrolysis such as ARL-67156 and POM-1 to suppress the catabolism of ATP and prolong its effects in pharmacological studies. Our aim was to investigate directly the effects of ARL-67156 and POM-1 on the degradation of ATP and ADP in mouse colonic muscles. Methods The degradation of ATP and ADP was evaluated by superfusing tissues with 1,N6-etheno-ATP (eATP) and 1,N6-etheno-ADP (eADP) as substrates and monitoring the decrease of substrate and increase of products (i.e., eADP, eAMP, and e-adenosine) by high-performance liquid chromatography techniques with fluorescence detection. Relaxation responses to etheno-derivatized and non-derivatized ATP and ADP were examined in isometric tension experiments. Key results ARL-67156 inhibits the degradation of ADP but not of ATP whereas POM-1 inhibits the degradation of ATP but not of ADP in murine colonic muscles. Consequently, ARL-67156 enhances relaxation responses to both ATP and ADP whereas POM-1 reduces relaxation to ATP and does not affect relaxation to ADP. Conclusions & Inferences Studies that use ARL-67156 to inhibit ATP degradation in smooth muscle likely evaluate responses to accumulated ADP rather than ATP. POM-1 appears to be a more selective inhibitor of ATP degradation in the mouse colon. The choice of pharmacological tools in studies on extracellular ATP signaling may affect the interpretation of experimental data in functional studies.

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ATP as a Co‐Transmitter with Noradrenaline in Sympathetic Nerves—Function and Fate

Cited by 16 publications

References 32 publications

Influence of purinergic modulators on eEPSCs in rat CA3 hippocampal neurons: Contribution of ionotropic ATP receptors

Influence of purinergic modulators on eEPSCs in rat CA3 hippocampal neurons: Contribution of ionotropic ATP receptors

Astrocytes in the damaged brain: Molecular and cellular insights into their reactive response and healing potential

A commonly used ecto‐ATPase inhibitor, ARL‐67156, blocks degradation of ADP more than the degradation of ATP in murine colon

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