Activation of metabotropic glutamate receptors increases extracellular adenosine in vivo

Bennett, H.J.; White, Thomas D.; Semba, Kazue

doi:10.1097/00001756-200011090-00018

Cited by 15 publications

(11 citation statements)

References 13 publications

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“…When adenosine biosensors were used, adenosine release could be observed (measuring ~2 µM in CA3) in response to DHPG-induced activity. Adenosine release in response to GI mGluR activation has previously been observed in vivo (Bennett et al, 2000) and in vitro (Sims et al, 2013), and is in line with the wide body of evidence that epileptic seizures or in vitro epileptiform activity is accompanied by a release of adenosine that limits seizure activity ).…”

Section: Purine Release During Mglur-dependent Oscillationssupporting

confidence: 84%

Pannexin-1-mediated ATP release from area CA3 drives mGlu5-dependent neuronal oscillations

2015

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The activation of Group I metabotropic glutamate receptors (GI mGluRs) in the hippocampus results in the appearance of persistent bursts of synchronised neuronal activity. Such activity is known to cause the release of the purines ATP and its neuroactive metabolite, adenosine.We have investigated the role of the purines in GI mGluR-induced oscillations in hippocampal areas CA3 and CA1 using pharmacological techniques and microelectrode biosensors for ATP and adenosine. The GI mGluR agonist DHPG induced both persistent oscillations in neuronal activity and the release of adenosine in areas CA1 and CA3. In contrast, the DHPG-induced release of ATP was only observed in area CA3. Whilst adenosine acting at adenosine A 1 receptors suppressed DHPG-induced burst activity, the activation of mGlu5 and P2Y 1 ATP receptors were necessary for the induction of DHPG-induced oscillations. Selective inhibition of pannexin-1 hemichannels with a low concentration of carbenoxolone (10 µM) or probenecid (1 mM) did not affect adenosine release in area CA3, but prevented both ATP release in area CA3 and DHPG-induced bursting. These data reveal key aspects of GI mGluR-dependent neuronal activity that are subject to bidirectional regulation by ATP and adenosine in the initiation and pacing of burst firing, respectively, and which have implications for the role of GI mGluRs in seizure activity and neurodevelopmental disorders.

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Section: Purine Release During Mglur-dependent Oscillationssupporting

confidence: 84%

Pannexin-1-mediated ATP release from area CA3 drives mGlu5-dependent neuronal oscillations

2015

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“…In vitro DNP increased adenosine concentrations in the hippocampal slice (Doolette, 1997). Brain extracellular adenosine levels increase as a response to electrical stimulation (Lloyd et al ., 1993), or to stimulation by glutamate or bicuculline (Winn et al ., 1980; Bennett et al ., 2000). Extracellular adenosine originates either from the dephosphorylation of adenine nucleotides in the extracellular space, or from the intracellular metabolism combined with rapid transport to the extracellular space in order to equilibrate the concentration difference (for a review, see Dunwiddie & Masino, 2001).…”

Section: Discussionmentioning

confidence: 99%

Local energy depletion in the basal forebrain increases sleep

Kalinchuk

Urrila

Alanko

et al. 2003

Eur J of Neuroscience

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Sleep saves energy, but can brain energy depletion induce sleep? We used 2,4-dinitrophenol (DNP), a molecule which prevents the synthesis of ATP, to induce local energy depletion in the basal forebrain of rats. Three-hour DNP infusions induced elevations in extracellular concentrations of lactate, pyruvate and adenosine, as well as increases in non-REM sleep during the following night. Sleep was not affected when DNP was administered to adjacent brain areas, although the metabolic changes were similar. The amount and the timing of the increase in non-REM sleep, as well as in the concentrations of lactate, pyruvate and adenosine with 0.5-1.0 mM DNP infusion, were comparable to those induced by 3 h of sleep deprivation. Here we show that energy depletion in localized brain areas can generate sleep. The energy depletion model of sleep induction could be applied to in vitro research into the cellular mechanisms of prolonged wakefulness.

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“…In principle, PTD could result from postsynaptic changes in AMPA receptors (see Nakazawa et al ., 1995) or it could reflect a presynaptic effect, for example following release of nitric oxide (Casado et al . 2000), adenosine (Bennett et al . 2000) or cannabinoids (Kreitzer & Regehr, 2001).…”

Section: Discussionmentioning

confidence: 99%

“…In principle, PTD could result from postsynaptic changes in AMPA receptors (see Nakazawa et al, 1995) or it could re¯ect a presynaptic effect, for example following release of nitric oxide (Casado et al 2000), adenosine (Bennett et al 2000) or cannabinoids (Kreitzer & Regehr, 2001). With the sharp microelectrode current clamp recording technique used here, conventional tests of whether the mGlu The hyperpolarization seen after the ®rst stimulus was elicited by a current step (as indicated by the scheme given below the lower trace), which was imposed in order to monitor the bridge balance and cell input resistance.…”

Section: Role Of Mglu Receptors In Post-tetanic Depressionmentioning

confidence: 99%

mGlu1 receptors mediate a post‐tetanic depression at parallel fibre–Purkinje cell synapses in rat cerebellum

Neale

Garthwaite

Batchelor

2001

Eur J of Neuroscience

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Metabotropic glutamate (mGlu) receptors are located pre- and postsynaptically at central synapses. Activation of the receptors by exogenous agonists usually results in a reversible depression of fast glutamatergic neurotransmission. Evidence that synaptically released glutamate has such an action, however, is scarce. Sharp microelectrode recordings were used to investigate the modulatory role of mGlu receptors at a well-studied glutamatergic synapse, the one between parallel fibres and Purkinje cells in rat cerebellar slices. Brief, tetanic stimulation of the parallel fibres caused a depression of subsequent fast EPSPs. This post-tetanic depression (PTD) reached its maximum 4.5 s after the tetanus. Measured at this point, PTD was frequency-dependent; 10 stimuli at 20 Hz produced no significant depression, whereas, at 100 Hz the same number of stimuli was maximally effective (approximately 50% depression). The nonselective mGlu antagonist, (S)-alpha-methyl-4-carboxyphenylglycine 1 mm or the GABAB antagonist, CGP35348 (1 mm), both decreased the magnitude of the PTD. In the presence of CGP35348 the mGlu1 antagonist, 7-hydroxyiminocyclopropan[b]chromen-1a-carboxylic acid ethyl ester (300 microm), inhibited PTD further. A group II/III mGlu antagonist had no effect. These observations indicate that synaptically activated mGlu1 receptors not only generate a slow EPSP and induce Ca2+ mobilization in Purkinje cells, as reported previously, but also produce a transient depression of fast synaptic transmission. This short-term plasticity may be important for shaping the output of cerebellar circuits and/or it could provide a substrate for long-term depression when additional mechanisms are superimposed.

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Activation of metabotropic glutamate receptors increases extracellular adenosine in vivo

Cited by 15 publications

References 13 publications

Pannexin-1-mediated ATP release from area CA3 drives mGlu5-dependent neuronal oscillations

Pannexin-1-mediated ATP release from area CA3 drives mGlu5-dependent neuronal oscillations

Local energy depletion in the basal forebrain increases sleep

mGlu1 receptors mediate a post‐tetanic depression at parallel fibre–Purkinje cell synapses in rat cerebellum

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