ATP-induced in vivo neurotoxicity in the rat striatum via P2 receptors

Jae K. Ryu; Jean Kim; Sang H. Choi; Young J. Oh; Yong B. Lee; Seung U. Kim; Byung K. Jin

doi:10.1097/00001756-200209160-00008

ATP-induced in vivo neurotoxicity in the rat striatum via P2 receptors

Jae K. Ryu, Jean Kim, Sang H. Choi, Young J. Oh, Yong B. Lee, Seung U. Kim, Byung K. Jin

Department of Systems Biology

Research output: Contribution to journal › Article › peer-review

70 Citations (Scopus)

Abstract

The present study examined the in vivo effects of ATP on the striatum of Sprague-Dawley rats. Intrastriatal administration of ATP produced dose-dependent striatal lesions as confirmed by cresyl violet staining. Additional immunostaining using neuronal nuclear protein (NeuN), OX-42 and GFAP antibodies revealed that ATP caused death of both neurons and glial cells. The nonmetabolizable ATP analogue ATPγS and P2X receptor agonist α,β-methylene ATP (α,β-MeATP) mimicked ATP effects, whereas either P2Y receptor agonist ADP or PI receptor agonist adenosine did not. The P2 receptor antagonist reactive blue 2, but not pyridoxal-phosphate-6-azophenyl-2′,4′-disulphonic acid (PPADS) attenuated ATP-induced striatal injury. These results suggest that intrastriatal administration of ATP causes P2X receptor-mediated cell death in the striatum and support the hypothesis that extracellular ATP can be an important mediator of neuropathological events of brain injuries.

Original language	English
Pages (from-to)	1611-1615
Number of pages	5
Journal	NeuroReport
Volume	13
Issue number	13
DOIs	https://doi.org/10.1097/00001756-200209160-00008
Publication status	Published - 2002 Sept 16

All Science Journal Classification (ASJC) codes

Neuroscience(all)

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10.1097/00001756-200209160-00008

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title = "ATP-induced in vivo neurotoxicity in the rat striatum via P2 receptors",

abstract = "The present study examined the in vivo effects of ATP on the striatum of Sprague-Dawley rats. Intrastriatal administration of ATP produced dose-dependent striatal lesions as confirmed by cresyl violet staining. Additional immunostaining using neuronal nuclear protein (NeuN), OX-42 and GFAP antibodies revealed that ATP caused death of both neurons and glial cells. The nonmetabolizable ATP analogue ATPγS and P2X receptor agonist α,β-methylene ATP (α,β-MeATP) mimicked ATP effects, whereas either P2Y receptor agonist ADP or PI receptor agonist adenosine did not. The P2 receptor antagonist reactive blue 2, but not pyridoxal-phosphate-6-azophenyl-2′,4′-disulphonic acid (PPADS) attenuated ATP-induced striatal injury. These results suggest that intrastriatal administration of ATP causes P2X receptor-mediated cell death in the striatum and support the hypothesis that extracellular ATP can be an important mediator of neuropathological events of brain injuries.",

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AU - Ryu, Jae K.

AU - Kim, Jean

AU - Choi, Sang H.

AU - Oh, Young J.

AU - Lee, Yong B.

AU - Kim, Seung U.

AU - Jin, Byung K.

PY - 2002/9/16

Y1 - 2002/9/16

N2 - The present study examined the in vivo effects of ATP on the striatum of Sprague-Dawley rats. Intrastriatal administration of ATP produced dose-dependent striatal lesions as confirmed by cresyl violet staining. Additional immunostaining using neuronal nuclear protein (NeuN), OX-42 and GFAP antibodies revealed that ATP caused death of both neurons and glial cells. The nonmetabolizable ATP analogue ATPγS and P2X receptor agonist α,β-methylene ATP (α,β-MeATP) mimicked ATP effects, whereas either P2Y receptor agonist ADP or PI receptor agonist adenosine did not. The P2 receptor antagonist reactive blue 2, but not pyridoxal-phosphate-6-azophenyl-2′,4′-disulphonic acid (PPADS) attenuated ATP-induced striatal injury. These results suggest that intrastriatal administration of ATP causes P2X receptor-mediated cell death in the striatum and support the hypothesis that extracellular ATP can be an important mediator of neuropathological events of brain injuries.

AB - The present study examined the in vivo effects of ATP on the striatum of Sprague-Dawley rats. Intrastriatal administration of ATP produced dose-dependent striatal lesions as confirmed by cresyl violet staining. Additional immunostaining using neuronal nuclear protein (NeuN), OX-42 and GFAP antibodies revealed that ATP caused death of both neurons and glial cells. The nonmetabolizable ATP analogue ATPγS and P2X receptor agonist α,β-methylene ATP (α,β-MeATP) mimicked ATP effects, whereas either P2Y receptor agonist ADP or PI receptor agonist adenosine did not. The P2 receptor antagonist reactive blue 2, but not pyridoxal-phosphate-6-azophenyl-2′,4′-disulphonic acid (PPADS) attenuated ATP-induced striatal injury. These results suggest that intrastriatal administration of ATP causes P2X receptor-mediated cell death in the striatum and support the hypothesis that extracellular ATP can be an important mediator of neuropathological events of brain injuries.

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ATP-induced in vivo neurotoxicity in the rat striatum via P2 receptors

Abstract

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