Action of externally applied ATP on rat reticulospinal vasomotor neurons

Sun, Miao Kun; Wahlestedt, Claes; Reis, Donald J.

doi:10.1016/0014-2999(92)94824-f

Cited by 58 publications

(37 citation statements)

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“…Extracellular ATP induces various biological responses such as excitability of spinal cord neurons [3], proliferation of astrocytes [4], inhibition of starvationinduced apoptosis in PC 12 cells [5], and modulation of neurotransmission [6]. These diverse biological actions are mediated by the activation of cell surface receptors including ligand-gated ion channels (P2X) and G-protein coupled (P2Y) receptor subtypes [7].…”

Section: Introductionmentioning

confidence: 99%

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

et al. 2002

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The present study examined the in vivo e¡ects of ATP on the striatum of Sprague^Dawley rats. Intrastriatal administration of ATP produced dose-dependent striatal lesions as con¢rmed 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 ATPgS and P2X receptor agonist a,b-methylene ATP (a,b-MeATP) mimicked ATP e¡ects, whereas either P2Y receptor agonist ADP or P1 receptor agonist adenosine did not. The P2 receptor antagonist reactive blue 2, but not pyridoxal-phosphate-6 -azophenyl-2 0 ,4 0 -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. NeuroReport13:1611^1615

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Section: Introductionmentioning

confidence: 99%

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

et al. 2002

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“…In vitro, loose-patch recordings from RTN neurons show that P2 receptor blockers decreased responsiveness to both 10% and 15% CO 2 also by 30%. In the slice, the contribution of purinergic signalling to RTN chemoreception did not increase with temperature (22)(23)(24)(25)(26)(27)(28)(29)(30)(31)(32)(33)(34)(35) • C) and was retained in low extracellular Ca 2+ medium. Conversely, the gap junction blockers carbenoxolone and cobalt decreased neuronal CO 2 /H + sensitivity by an amount similar to P2 receptor antagonists.…”

Section: Key Pointsmentioning

confidence: 95%

“…19 In addition, presym pathetic neurons in the RVLM are activated by exogenous application of ATP analogs, 26,29,30 and application of puri nergic agonists into this region increased sympathetic tone 29 and blood pressure 29,30 in anesthetized rats. Furthermore, inhibition of P2X receptors within the more caudal RVLM (at the level of the Bötzinger complex) blunted the ventila tory, but not pressure response elicited by peripheral che moreceptor activation in conscious rats.…”

Section: P2y1 Receptors Regulate the Peripheral Chemoreflex At The Lementioning

confidence: 99%

“…9,18 However, purinergic signaling has also been impli cated in the peripheral chemoreflex, [19][20][21][22] including at the level of the RVLM. 23 For example, chemosensitive RTN neurons 24,25 and presympathetic RVLM neurons 26 are activated by puriner gic agonists, application of purinergic agonists into the RVLM increased breathing 27,28 and blood pressure 29,30 in anesthetized rats, and inhibition of P2 receptors in the nearby Bötzinger and Abstract-Catecholaminergic C1 cells of the rostral ventrolateral medulla (RVLM) are key determinants of the sympathoexcitatory response to peripheral chemoreceptor activation. Overactivation of this reflex is thought to contribute to increased sympathetic activity and hypertension; however, molecular mechanisms linking peripheral chemoreceptor drive to hypertension remain poorly understood.…”

Section: Role Of Astrocytes In Rtn Purinergic Signallingmentioning

confidence: 99%

“…49,50 Also consistent with a role of puri nergic signaling in peripheral chemoreflex, cNTS injections of glutamate receptor antagonists did not block sympathetic or bradycardic components of the chemoreceptor reflex in awake rats 51 or in the working heartbrain stem prepara tion, 52 whereas simultaneous antagonism of glutamate and P2 receptors in this region reduced pressor and sympathetic responses to chemoreflex activation. 19 In addition, presym pathetic neurons in the RVLM are activated by exogenous application of ATP analogs, 26,29,30 and application of puri nergic agonists into this region increased sympathetic tone 29 and blood pressure 29,30 in anesthetized rats. Furthermore, inhibition of P2X receptors within the more caudal RVLM (at the level of the Bötzinger complex) blunted the ventila tory, but not pressure response elicited by peripheral che moreceptor activation in conscious rats.…”

Section: P2y1 Receptors Regulate the Peripheral Chemoreflex At The Lementioning

confidence: 99%

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Mecanismos purinérgicos no bulbo ventrolateral rostral modulam respostas cardiovasculares e respiratórias promovidas pela ativação dos quimiorreceptores centrais e periféricos.

Sobrinho¹

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AGRADECIMENTOSAo meu orientador, Prof. Dr. Thiago S. Moreira, pela oportunidade, estimulação e apoio no desenvolvimento deste trabalho, mas também pela compreensão e pela ótima convivência.A Prof.a Dra. Ana Carolina Takakura, que juntamente ao Prof. Thiago desde o ínicio oferecem suporte para meu crecimento cientifico, mas também pela inspiração pessoal, pois ambos representam exemplos de dedicação.Aos Professores Dr. Vagner Antunes, Dra. Renata Frazão e a Dra. Mirian Bassi, examinadores no exame de qualificação, pela discussão e contribuição.Aos professores presentes na banca examinadora de defesa, pela avaliação, leitura e atenção dispensada. Aos membros do Laboratório de Controle Cardiorrespiratório e do Laboratório deControle Neural Cardiorrespiratório, Leonardo, Thales, Milene, Rosélia, Bárbara, Janayna, Elvis, Talita, Thais, Josiane, Fabiana, Luiz, Silvio, Marina e Karen, pelas horas de convivência, pelos conhecimentos transferidos, pelas discussões e horas de descontração.Ao Instituto de Ciências Biomédicas e aos funcionários dos mais diversificados setores, sempre solícitos e de crucial importância para o andamento e finalização deste trabalho, em especial para Adilson Alves, Ana Maria Campos, Julieta Scialfa e Mônica Amaral, pela amizade e suporte técnico.Aos professores Fernando Abdukader, Luiz R. G. Britto, Sara J. Shammah Lagnado e Martin A. Metzger que me prestaram total apoio sempre que requisitados.Ao meu pai José Miguel Sobrinho, minha irmã Denise, meu cunhado José Fernando e especialmente ao meu sobrinho Estevão, pelo apoio e carinho nos momentos mais difíceis.A minha querida Helena Panizza, pelo carinho, compreensão e apoio, e a sua família Sr.Cezar, Sra. Ana, Julia e meu amigo Theo pela companhia e acolhimento. Quimiorrecepção é o mecanismo pelo qual células especializadas detectam variações nos níveis de CO2, O2 e H + presentes no sangue, liquor e parênquima, onde dois sistemas principais são reconhecidos: quimiorreceptores periféricos, localizados na bifurcação da aorta e no corpúsculo carotídeo e quimiorreceptores centrais, representados por grupamentos de neurônios especializados em detectar apenas as variações de CO2/H + . Em comum, estas estruturas informam centros respiratórios e simpáticos no sistema nervoso central (SNC) gerando ajustes da atividade cardiorrespiratória. A região ventrolateral do bulbo contém neurônios bulbo-espinais que modulam atividade simpática (grupamento C1) e neurônios quimiossensíveis localizados no núcleo retrotrapezóide (RTN). Adicionalmente a quimiorrecepção intrínseca dos neurônios do RTN, tem sido demonstrado que outras células nesta região (possivelmente astrócitos) atuam como sensores de CO2/H + , liberando ATP para promover a ativação de neurônios via receptores purinérgicos P2, na tentativa de promover ajustes cardiorrespiratórios. No presente trabalho, ultilizamos ratos Wistar adultos, anestesiados e ventilados artificialmente para avaliar a ação da sinalização purinérgica em regiões encefálicas com características quimiossensíveis bem como o envolvim...

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Distribution of the P2X2 receptor subunit of the ATP-gated ion channels in the rat central nervous system

et al. 1999

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The distribution of the P2X2 receptor subunit of the adenosine 5′‐triphosphate (ATP)‐gated ion channels was examined in the adult rat central nervous system (CNS) by using P2X2 receptor‐specific antisera and riboprobe‐based in situ hybridisation. P2X2 receptor mRNA expression matched the P2X2 receptor protein localisation. An extensive expression pattern was observed, including: olfactory bulb, cerebral cortex, hippocampus, habenula, thalamic and subthalamic nuclei, caudate putamen, posteromedial amygdalo‐hippocampal and amygdalo‐cortical nuclei, substantia nigra pars compacta, ventromedial and arcuate hypothalamic nuclei, supraoptic nucleus, tuberomammillary nucleus, mesencephalic trigeminal nucleus, dorsal raphe, locus coeruleus, medial parabrachial nucleus, tegmental areas, pontine nuclei, red nucleus, lateral superior olive, cochlear nuclei, spinal trigeminal nuclei, cranial motor nuclei, ventrolateral medulla, area postrema, nucleus of solitary tract, and cerebellar cortex. In the spinal cord, P2X2 receptor expression was highest in the dorsal horn, with significant neuronal labeling in the ventral horn and intermediolateral cell column. The identification of extensive P2X2 receptor immunoreactivity and mRNA distribution within the CNS demonstrated here provides a basis for the P2X receptor antagonist pharmacology reported in electrophysiological studies. These data support the role for extracellular ATP acting as a fast neurotransmitter at pre‐ and postsynaptic sites in processes such as sensory transmission, sensory‐motor integration, motor and autonomic control, and in neuronal phenomena such as long‐term potentiation (LTP) and depression (LTD). Additionally, labelling of neuroglia and fibre tracts supports a diverse role for extracellular ATP in CNS homeostasis. J. Comp. Neurol. 407:11–32, 1999. © 1999 Wiley‐Liss, Inc.

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Action of externally applied ATP on rat reticulospinal vasomotor neurons

Cited by 58 publications

References 10 publications

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

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

Mecanismos purinérgicos no bulbo ventrolateral rostral modulam respostas cardiovasculares e respiratórias promovidas pela ativação dos quimiorreceptores centrais e periféricos.

Distribution of the P2X2 receptor subunit of the ATP-gated ion channels in the rat central nervous system

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