Release of adenosine 5′-triphosphate from synaptosomes from different regions of rat brain

Potter, Pamela E.; White, Thomas D.

doi:10.1016/0306-4522(80)90207-9

Cited by 92 publications

(31 citation statements)

References 34 publications

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“…Although it has been demonstrated that ATP is stored in synaptic vesicles and that it is exocytotically released, it is only recently that the role of ATP as a neurotransmitter in the central nervous system has been determined (White, 1977;Potter & White, 1980). Since then ATP has been shown to activate ionic currents in central neurones (Ueno et al, 1992;Shen & North, 1993;Illes & Norenberg, 1993); only by means of the trypanocide, suramin, a P2-purinoceptor antagonist (Hoyle, 1990), was it possible to demonstrate that central synapses use ATP as a fast excitatory neurotransmitter (Edwards et al, 1992).…”

Section: Introductionmentioning

confidence: 99%

A novel receptor for diadenosine polyphosphates coupled to calcium increase in rat midbrain synaptosomes

Pintor

Miras‐Portugal

1995

British J Pharmacology

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1 Diadenosine polyphosphates, Ap4A and Ap5A, as well as ATP, c,fl-MeATP and ADP-P-S, were able to elicit variable intrasynaptosomal Ca21 increases in rat midbrain synaptic terminals. The origin of the Ca2+ increment was the extrasynaptosomal space since the elimination of extracellular Ca2+ abolished the effect of all the agonists. 2 The P2-purinoceptor antagonist, suramin, did not affect the Ca2+-increase evoked by diadenosine polyphosphates but dramatically blocked the Ca2+ entry induced by ATP and its synthetic analogues. 3 The actions of Ap5A and ATP on the intrasynaptosomal Ca21 increase did not cross-desensitize. 4 Concentration-response studies for diadenosine polyphosphates showed pD2 values of 54.5 ± 4.2 uM and 55.6 ± 3.8 yM for Ap4A and Ap5A, respectively. 5 The entry of calcium induced by diadenosine polyphosphates could be separated into two components. The first represented a selective voltage-independent Ca2+ entry; the second, a sustained phase which was voltage-dependent. 6 Studies on the voltage-dependent Ca2 +-channels involved in the effects of the diadenosine polyphosphates, demonstrated that o-conotoxin G-VI-A inhibited the sustained Ca2+-entry, suggesting the participation of an N-type Ca2+-channel. This toxin was unable to abolish the initial cation entry induced by Ap4A or ApNA. co-Agatoxin IV-A, tetrodotoxin, or nifedipine did not inhibit the effects of the diadenosine polyphosphates. 7 The effect of ATP on Ca2+-entry was abolished by nifedipine and co-conotoxin G-VI-A, suggesting the participation of L-and N-type Ca2"-channels in the response to ATP.8 These data suggest that Ap4A, Ap5A and ATP activate the same intracellular Ca21 signal through different receptors and different mechanisms. Ap4A and Ap5A induce a more selective Ca2+-entry in a voltage-independent process. This is the first time that a selective action of diadenosine polyphosphate through receptors other than PI and P2-purinoceptors has been described.

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Section: Introductionmentioning

confidence: 99%

A novel receptor for diadenosine polyphosphates coupled to calcium increase in rat midbrain synaptosomes

Pintor

Miras‐Portugal

1995

British J Pharmacology

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“…In fact, there is a clear frequency-dependent increase in the nerve-evoked release of ATP and the consecutive stimulation of the same preparations with increasing frequencies of stimulation triggers the release of increasing amounts of ATP. It is also interesting to note that the absolute amounts of ATP detected in the bath of stimulated hemidiaphragm preparations are larger than these recorded in hippocampal or cortical preparations [6,13]. This larger release of ATP at neuromuscular synapses might be a consequence of the significant contribution of activated muscle fibres for the nerve-evoked ATP release.…”

mentioning

confidence: 93%

ATP is released from nerve terminals and from activated muscle fibres on stimulation of the rat phrenic nerve

Santos

Salgado

Cunha

2003

Neuroscience Letters

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Nerve stimulation increases the concentration of ATP in the synaptic cleft, which can act as a neurotransmitter or as a presynaptic neuromodulator. Using the luciferin-luciferase assay, we observed that the extracellular concentration of ATP increased by 11 -26 nM over a basal concentration of 6 nM, in a frequency dependent manner (1 -5 Hz), in the adult rat phrenic nerve-hemidiaphragm preparation. This ATP release depends on nerve activity since it was abolished by tetrodotoxin (1 mM) and is strictly dependent on the presence of extracellular calcium. However, more than half of this nerve-evoked release of ATP is derived from activated muscle fibres since the selective postsynaptic nicotinic receptor antagonist, a-bungarotoxin (1 mM), inhibited by over 60% the evoked release of ATP. The presently observed post-synaptic release of ATP together with the previously reported lack of post-synaptic effects of ATP and to the ability of ATP to act as a presynaptic modulator open the possibility that ATP may behave as a retrograde messenger at this neuromuscular junction. q

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“…Once released, nucleotides elicit a variety of biological responses to regulate cellular function (1,2). Endogenous nucleotides were found to be released from different brain regions, and cerebral blood vessels were found to be more sensitive to nucleotides than non-cerebral vessels (3,4). Furthermore, in response to hypoxia and shear stress, nucleotides are released from erythrocytes, leukocytes, platelets, and activated endothelial cells.…”

Section: Introductionmentioning

confidence: 99%

Mechanism Underlying Endothelium-Dependent Relaxation by 2-Methylthio-ADP in Monkey Cerebral Artery

et al. 2010

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Abstract.We recently reported endothelium-dependent relaxation caused by nucleotides in the non-human primate cerebral artery. Here, we investigated the endothelium-dependent, nitric oxide-and prostanoid-independent relaxation induced by 2-methylthio-ADP (2MeSADP) in monkey cerebral artery. Mechanical responses of isolated monkey cerebral arteries to the agents were isometrically recorded. In endothelium-intact arterial strips treated with indomethacin plus N G -nitro-L-arginine and partially contracted with prostaglandin F 2α , 2MeSADP (1 nM -10 μM) induced concentration-dependent relaxation that was abolished by removal of endothelium but was not influenced by either carboxy PTIO or 18α-glycyrrhetinic acid. The 2MeSADP-induced relaxation was inhibited by MRS2179 and U73122. The relaxation was markedly suppressed by exposure of the strips to high K + media, but was not affected by glibenclamide. Combination of charybdotoxin plus apamin markedly suppressed the relaxation, whereas iberiotoxin partially attenuated it. Relaxation induced by 2MeSADP was inhibited by arachidonyl trifluoromethyl ketone, ketoconazole, and 14,15-epoxyeicosa-5(Z)-enoic acid. The inhibitors that affected the 2MeSADP-induced relaxation did not influence relaxation caused by sodium nitroprusside or forskolin. These findings indicate that 2MeSADP elicits 'endothelium-derived hyperpolarizing factor (EDHF)-type' relaxation via stimulation of endothelial P2Y 1 receptors in monkey cerebral artery. Furthermore, phospholipase A 2 , cytochrome P450-derived epoxyeicosatrienoic acids and Ca 2+-activated K + channels appear to be involved in the relaxation.

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Release of adenosine 5′-triphosphate from synaptosomes from different regions of rat brain

Cited by 92 publications

References 34 publications

A novel receptor for diadenosine polyphosphates coupled to calcium increase in rat midbrain synaptosomes

A novel receptor for diadenosine polyphosphates coupled to calcium increase in rat midbrain synaptosomes

ATP is released from nerve terminals and from activated muscle fibres on stimulation of the rat phrenic nerve

Mechanism Underlying Endothelium-Dependent Relaxation by 2-Methylthio-ADP in Monkey Cerebral Artery

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