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Bruno G. Frenguelli

Researcher at University of Warwick

Publications -  94
Citations -  7723

Bruno G. Frenguelli is an academic researcher from University of Warwick. The author has contributed to research in topics: Adenosine & Adenosine A1 receptor. The author has an hindex of 34, co-authored 85 publications receiving 7180 citations. Previous affiliations of Bruno G. Frenguelli include University of Bristol & University of Dundee.

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Deficient long-term memory in mice with a targeted mutation of the cAMP-responsive element-binding protein

TL;DR: Consistent with models claiming a role for long-term potentiation (LTP) in memory, LTP in hippocampal slices from CREB mutants decayed to baseline 90 min after tetanic stimulation, however, paired-pulse facilitation and posttetanic potentiation are normal.
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Calmodulin-dependent protein kinase kinase-β is an alternative upstream kinase for AMP-activated protein kinase

TL;DR: It is reported that there is a significant basal activity and phosphorylation of AMPK in LKB1-deficient cells that can be stimulated by Ca2+ ionophores, and studies using the CaMKK inhibitor STO-609 and isoform-specific siRNAs show thatCaMKKbeta is required for this effect.
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Mitochondrial Membrane Potential and Glutamate Excitotoxicity in Cultured Cerebellar Granule Cells

TL;DR: It is concluded that transient Ca2+loading of mitochondria as a consequence of NMDA receptor activation initiates oxidative damage to both plasma membrane Ca 2+ extrusion pathways and the inhibition of mitochondrial respiration.
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Characterization of Ca2+ signals induced in hippocampal CA1 neurones by the synaptic activation of NMDA receptors.

TL;DR: Tetanic stimulation of the Schaffer collateral‐commissural pathway resulted in compound EPSPs and excitatory postsynaptic currents (EPSCs) and somatic Ca2+ transients, respectively, under current‐ and voltage‐clamp conditions.
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Temporal and mechanistic dissociation of ATP and adenosine release during ischaemia in the mammalian hippocampus.

TL;DR: The data suggest that ATP and adenosine release during ischaemia are for the most part independent processes with distinct underlying mechanisms and will consequently confer temporally distinct influences on neuronal and glial function in the ischaemic brain.