ATP extracellular concentrations are increased in the rat striatum during in vivo ischemia

Melani, Alessia; Turchi, D.; Vannucchi, Maria Giuliana; Cipriani, Sara; Gianfriddo, Marco; Pedata, Felicita

doi:10.1016/j.neuint.2005.05.014

Cited by 236 publications

(190 citation statements)

References 40 publications

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“…Increases in the metabolism of ATP may be part of pathogenic processes manifesting during the initial phase of pilocarpine-induced TLE. This hypothesis is in agreement with previous studies demonstrating liberation of ATP and adenosine following brain insult [23,24]. Further, it was postulated that ATP and adenosine could mediate antagonistic actions.…”

Section: Discussionsupporting

confidence: 92%

Variations of ATP and its metabolites in the hippocampus of rats subjected to pilocarpine-induced temporal lobe epilepsy

Doná

Conceição

Ulrich

et al. 2016

Purinergic Signalling

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Although purinergic receptor activity has lately been associated with epilepsy, little is known about the exact role of purines in epileptogenesis. We have used a rat model of temporal lobe epilepsy induced by pilocarpine to study the dynamics of purine metabolism in the hippocampus during different times of status epilepticus (SE) and the chronic phase. Concentrations of adenosine 5′-triphosphate (ATP), adenosine diphosphate (ADP), adenosine monophosphate (AMP), and adenosine in normal and epileptic rat hippocampus were determined by microdialysis in combination with high-performance liquid chromatography (HPLC). Extracellular ATP concentrations did not vary along 4 h of SE onset. However, AMP concentration was elevated during the second hour, whereas ADP and adenosine concentrations augmented during the third and fourth hour following SE. During chronic phase, extracellular ATP, ADP, AMP, and adenosine concentrations decreased, although these levels again increased significantly during spontaneous seizures. These results suggest that the increased turnover of ATP during the acute period is a compensatory mechanism able to reduce the excitatory role of ATP. Increased adenosine levels following 4 h of SE may contribute to block seizures. On the other hand, the reduction of purine levels in the hippocampus of chronic epileptic rats may result from metabolic changes and be part of the mechanisms involved in the onset of spontaneous seizures. This work provides further insights into purinergic signaling during establishment and chronic phase of epilepsy.

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Section: Discussionsupporting

confidence: 92%

Variations of ATP and its metabolites in the hippocampus of rats subjected to pilocarpine-induced temporal lobe epilepsy

Doná

Conceição

Ulrich

et al. 2016

Purinergic Signalling

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“…Energized glial mitochondria reverse brain damage W Zheng et al stimulation. 11 It is also clear that extracellular ATP concentrations are increased following ischemia, 28 which would be expected to activate purinergic receptors in astrocytes. Taken together, these data are consistent with an endogenous neuroprotective mechanism in astrocytes activated after ischemia, inhibited by disruption of either basal IP 3 R signaling or mitochondrial function and mediated, at least in part, by naturally stimulated P2Y 1 Rs.…”

Section: Discussionmentioning

confidence: 99%

P2Y₁R-Initiated, IP₃R-Dependent Stimulation of Astrocyte Mitochondrial Metabolism Reduces and Partially Reverses Ischemic Neuronal Damage in Mouse

Zheng

Watts

Holstein

et al. 2013

J Cereb Blood Flow Metab

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Glia-based neuroprotection strategies are emerging as promising new avenues to treat brain damage. We previously reported that activation of the glial-specific purinergic receptor, P2Y 1 R, reduces both astrocyte swelling and brain infarcts in a photothrombotic mouse model of stroke. These restorative effects were dependent on astrocyte mitochondrial metabolism. Here, we extend these findings and report that P2Y 1 R stimulation with the purinergic ligand 2-methylthioladenosine 5 0 diphosphate (2MeSADP) reduces and partially reverses neuronal damage induced by photothrombosis. In vivo neuronal morphology was confocally imaged in transgenic mice expressing yellow fluorescent protein under the control of the Thy1 promoter. Astrocyte mitochondrial membrane potentials, monitored with the potential sensitive dye tetra-methyl rhodamine methyl ester, were depolarized after photothrombosis and subsequently repolarized when P2Y 1 Rs were stimulated. Mice deficient in the astrocyte-specific type 2 inositol 1,4,5 trisphosphate (IP 3 ) receptor exhibited aggravated ischemic dendritic damage after photothrombosis. Treatment of these mice with 2MeSADP did not invoke an intracellular Ca 2 þ response, did not repolarize astrocyte mitochondria, and did not reduce or partially reverse neuronal lesions induced by photothrombotic stroke. These results demonstrate that IP 3 -Ca 2 þ signaling in astrocytes is not only critical for P2Y 1 R-enhanced protection, but suggest that IP 3 -Ca 2 þ signaling is also a key component of endogenous neuroprotection.

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“…What's more, ATP at 100 μM could induce OPC migration through P2Y1 receptors [12]. The ATP concentration the authors used was much higher than that in the extracellular space under physiological conditions, which is in the nanomolar level [51]. But, as we mentioned earlier, only when the ATP concentration is greater than 100 μM, can P2X7 receptors be activated [52].…”

Section: Discussionmentioning

confidence: 92%

P2X7 receptors and Fyn kinase mediate ATP-induced oligodendrocyte progenitor cell migration

Feng

Gao

et al. 2015

Purinergic Signalling

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Recruitment of oligodendrocyte precursor cells (OPCs) to the lesions is the most important event for remyelination after central nervous system (CNS) injury or in demyelinating diseases. However, the underlying molecular mechanism is not fully understood. In the present study, we found high concentrations of ATP could increase the number of migrating OPCs in vitro, while after pretreatment with oxidized ATP (a P2X7 receptor antagonist), the promotive effect was attenuated. The promotive effect of 2′(3′)-O-(4-benzoylbenzoyl) adenosine 5′-triphosphate (BzATP) (a P2X7 receptor agonist) was more potent than ATP. After incubation with BzATP, the activity of Fyn, one member of the Src family of kinases, was enhanced. Moreover, the interaction between P2X7 and Fyn was identified by co-immunoprecipitation. After blocking the activity of Fyn or downregulating the expression of Fyn, the migration of OPCs induced by BzATP was inhibited. These data indicate that P2X7 receptors/Fyn may mediate ATP-induced OPC migration under pathological conditions.

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ATP extracellular concentrations are increased in the rat striatum during in vivo ischemia

Cited by 236 publications

References 40 publications

Variations of ATP and its metabolites in the hippocampus of rats subjected to pilocarpine-induced temporal lobe epilepsy

Variations of ATP and its metabolites in the hippocampus of rats subjected to pilocarpine-induced temporal lobe epilepsy

P2Y₁R-Initiated, IP₃R-Dependent Stimulation of Astrocyte Mitochondrial Metabolism Reduces and Partially Reverses Ischemic Neuronal Damage in Mouse

P2X7 receptors and Fyn kinase mediate ATP-induced oligodendrocyte progenitor cell migration

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ATP extracellular concentrations are increased in the rat striatum during in vivo ischemia

Cited by 236 publications

References 40 publications

Variations of ATP and its metabolites in the hippocampus of rats subjected to pilocarpine-induced temporal lobe epilepsy

Variations of ATP and its metabolites in the hippocampus of rats subjected to pilocarpine-induced temporal lobe epilepsy

P2Y1R-Initiated, IP3R-Dependent Stimulation of Astrocyte Mitochondrial Metabolism Reduces and Partially Reverses Ischemic Neuronal Damage in Mouse

P2X7 receptors and Fyn kinase mediate ATP-induced oligodendrocyte progenitor cell migration

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P2Y₁R-Initiated, IP₃R-Dependent Stimulation of Astrocyte Mitochondrial Metabolism Reduces and Partially Reverses Ischemic Neuronal Damage in Mouse