Characterisation of ATP-induced facilitation of transmission in rat hippocampus

O’Kane, E.M.; Stone, T.W.

doi:10.1016/s0014-2999(00)00785-8

Cited by 22 publications

(26 citation statements)

References 53 publications

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“…A credible alternative might be that the neuromodulatory role of P2 receptors in glutamatergic synapses might not be related to conditions of low-frequency stimulation, in which one would expect calcium influx through P2X receptors to be most effective, but might only come into play during bursts of actions potentials, in which one would expect this P2 receptor-mediated calcium entry to be overshadowed by the massive calcium influx and the effect of other facilitating factor. Accordingly, the most consistent modulatory role of P2 receptors has been found in the control of long-term potentiation (O'Kane andStone, 2000, Pankratov et al, 2002;Almeida et al, 2003). This is also in agreement with the finding that the release of ATP in hippocampal preparations increases disproportionally with increasing frequencies of nerve stimulation (Wieraszko et al, 1989;Cunha et al, 1996).…”

Section: Discussionsupporting

confidence: 61%

Dual Presynaptic Control by ATP of Glutamate Release via Facilitatory P2X₁, P2X_2/3, and P2X₃and Inhibitory P2Y₁, P2Y₂, and/or P2Y₄Receptors in the Rat Hippocampus

Rodrigues¹,

Almeida²,

Richardson³

et al. 2005

J. Neurosci.

198

168

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Section: Discussionsupporting

confidence: 61%

Dual Presynaptic Control by ATP of Glutamate Release via Facilitatory P2X₁, P2X_2/3, and P2X₃and Inhibitory P2Y₁, P2Y₂, and/or P2Y₄Receptors in the Rat Hippocampus

Rodrigues¹,

Almeida²,

Richardson³

et al. 2005

J. Neurosci.

198

168

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“…It is also possible to produce changes in synaptic strength by the application of drugs. In several studies, it has been reported that superfusion of ATP induces a long-term modification of synaptic strength Fujii et al, 1995;O'Kane and Stone, 2000). It has been recognized that ATP acts as a synaptic transmitter in the central nervous system, including hippocampus Zimmermann, 1994;Pankratov et al, 1999).…”

Section: Introductionmentioning

confidence: 99%

“…In previous studies on ATP-induced synaptic modification, applications of ATP were performed by superfusion Fujii et al, 1995;O'Kane and Stone, 2000). With this method, the possibility exists that ATP in the perfusion medium could influence not only the Schaffer collateral-CA1 synapse, but also other synapses widely.…”

Section: Introductionmentioning

confidence: 99%

Long‐term potentiation and long‐term depression induced by local application of ATP to hippocampal CA1 neurons of the Guinea pig

et al. 2002

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The present study has investigated the role of ATP in the induction of synaptic plasticity, using local application of ATP by picopump administration into the stratum radiatum of guinea pig hippocampal region CA1. Excitatory postsynaptic currents (EPSCs) evoked by stimulation of Schaffer collateral/commissural afferents synapsing on CA1 pyramidal cells of hippocampal slices were monitored in voltage-clamp mode, using whole-cell recording. Brief local application of ATP (1 mM) induced an inward current, usually consisting of early- and late-phase components. Because the late-phase component of an ATP-induced current was largely inhibited by Ca2+-free solution, this component is supposed to depend on extracellular Ca2+. After local application of ATP, long-term synaptic modification of EPSCs was induced: LTP was detected in neurons exhibiting a small late Ca2+ current, while LTD was obtained from recordings showing a large late Ca2+ current in response to ATP application. There was a statistically significant correlation between the magnitude of long-term plastic changes and the size of Ca2+ currents in response to ATP application. Furthermore, there was significant difference between the average size of the Ca2+ current in the LTP group and the size in the LTD group. These results suggest that a small Ca2+ influx in response to ATP application induces LTP, whereas a large one induces LTD in guinea pig hippocampal CA1 neurons.

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“…Both excitatory and inhibitory effects have been suggested in peripheral nerves, in ganglia, and in the brain (von Kugelgen et al, 1993(von Kugelgen et al, , 1994Boehm, 1999;O'Kane and Stone, 2000;Smith et al, 2001). For example, hippocampal synaptic transmission is inhibited not only by adenosine but also by ATP, cAMP, and numerous cAMP and ATP analogs Lee et al, 1981).…”

mentioning

confidence: 99%

Modulation of Hippocampal Glutamatergic Transmission by ATP Is Dependent on Adenosine A₁ Receptors

Masino

Diao²,

Illéš³

et al. 2002

J Pharmacol Exp Ther

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Excitatory glutamatergic synapses in the hippocampal CA1 region of rats are potently inhibited by purines, including adenosine, ATP, and ATP analogs. Adenosine A 1 receptors are known to mediate at least part of the response to adenine nucleotides, either because adenine nucleotides activate A 1 receptors directly, or activate them secondarily upon the nucleotides' conversion to adenosine. In the present studies, the inhibitory effects of adenosine, ATP, the purportedly stable ATP analog adenosine-5Ј-O-(3-thio)triphosphate (ATP␥S), and cyclic AMP were examined in mice with a null mutation in the adenosine A 1 receptor gene. ATP␥S displaced the binding of A 1 -selective ligands to intact brain sections and brain homogenates from adenosine A 1 receptor wild-type animals. In homogenates, but not in intact brain sections, this displacement was abolished by adenosine deaminase. In hippocampal slices from wild-type mice, purines abolished synaptic responses, but slices from mice lacking functional A 1 receptors showed no synaptic modulation by adenosine, ATP, cAMP, or ATP␥S. In slices from heterozygous mice the dose-response curve for both adenosine and ATP was shifted to the right. In all cases, inhibition of synaptic responses by purines could be blocked by prior treatment with the competitive adenosine A 1 receptor antagonist 8-cyclopentyltheophylline. Taken together, these results show that even supposedly stable adenine nucleotides are rapidly converted to adenosine at sites close to the A 1 receptor, and that inhibition of synaptic transmission by purine nucleotides is mediated exclusively by A 1 receptors.

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Characterisation of ATP-induced facilitation of transmission in rat hippocampus

Cited by 22 publications

References 53 publications

Dual Presynaptic Control by ATP of Glutamate Release via Facilitatory P2X₁, P2X_2/3, and P2X₃and Inhibitory P2Y₁, P2Y₂, and/or P2Y₄Receptors in the Rat Hippocampus

Dual Presynaptic Control by ATP of Glutamate Release via Facilitatory P2X₁, P2X_2/3, and P2X₃and Inhibitory P2Y₁, P2Y₂, and/or P2Y₄Receptors in the Rat Hippocampus

Long‐term potentiation and long‐term depression induced by local application of ATP to hippocampal CA1 neurons of the Guinea pig

Modulation of Hippocampal Glutamatergic Transmission by ATP Is Dependent on Adenosine A₁ Receptors

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Characterisation of ATP-induced facilitation of transmission in rat hippocampus

Cited by 22 publications

References 53 publications

Dual Presynaptic Control by ATP of Glutamate Release via Facilitatory P2X1, P2X2/3, and P2X3and Inhibitory P2Y1, P2Y2, and/or P2Y4Receptors in the Rat Hippocampus

Dual Presynaptic Control by ATP of Glutamate Release via Facilitatory P2X1, P2X2/3, and P2X3and Inhibitory P2Y1, P2Y2, and/or P2Y4Receptors in the Rat Hippocampus

Long‐term potentiation and long‐term depression induced by local application of ATP to hippocampal CA1 neurons of the Guinea pig

Modulation of Hippocampal Glutamatergic Transmission by ATP Is Dependent on Adenosine A1 Receptors

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Dual Presynaptic Control by ATP of Glutamate Release via Facilitatory P2X₁, P2X_2/3, and P2X₃and Inhibitory P2Y₁, P2Y₂, and/or P2Y₄Receptors in the Rat Hippocampus

Dual Presynaptic Control by ATP of Glutamate Release via Facilitatory P2X₁, P2X_2/3, and P2X₃and Inhibitory P2Y₁, P2Y₂, and/or P2Y₄Receptors in the Rat Hippocampus

Modulation of Hippocampal Glutamatergic Transmission by ATP Is Dependent on Adenosine A₁ Receptors