Extracellular adenosine levels in neostriatum and hippocampus during rest and activity periods of rats

Huston, J.P.; Haas, Helmut L.; Boix, Fernando; Pfister, M.; Decking, Ulrich K. M.; Schrader, Jürgen; Schwarting, Rainer K.W.

doi:10.1016/0306-4522(96)00021-8

Cited by 167 publications

(98 citation statements)

References 41 publications

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“…The results of the present study together with those of previous evidence (Fiebich et al 1996;Schwaninger et al 1997) suggest a relationship between the neuroprotective effects of adenosine and Il-6 and provide a potential explanation for the paradoxical finding that adenosine A 1 receptors are up-regulated after sleep deprivation (Yanik and Radulovacki 1987) and ECT (Newman et al 1984;Gleiter et al 1989;Angelatou et al1993;, despite the presence of increased adenosine concentrations under these conditions (Huston et al 1996;Porkka-Heiskanen et al 1997;Dragunow 1988).…”

Section: Discussionsupporting

confidence: 69%

“…While the upregulation by carbamazepine of adenosine A 1 receptors is readily comprehensible from carbamazepine's selective antagonistic effects on A 1 receptors (Clark and Post 1989;van Calker et al 1991;Biber et al 1996), the upregulation of A 1 receptors after ECT or sleep deprivation presents a paradox, since the increase in extracellular adenosine concentrations under these conditions (Huston et al 1996; Porkka-Heiskanen et al 1997; Dragunow 1988) should rather downregulate adenosine A 1 receptors (Hettinger et al 1998;Ruiz et al 1996).…”

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confidence: 99%

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Interleukin-6 Enhances Expression of Adenosine A1 Receptor mRNA and Signaling in Cultured Rat Cortical Astrocytes and Brain Slices

Biber

2001

Neuropsychopharmacology

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The inhibitory neuromodulator adenosine is released in the brain in high concentrations under conditions of exaggerated neuronal activity such as ischemia and seizures, or electroconvulsive treatment. By inhibiting neural overactivity, adenosine counteracts seizure activity and promotes neuronal survival. Since stimulation of adenosineAdenosine, as a metabolite of ATP, nature's general energy source, has acquired early in evolution the general function of signaling and counteracting a dysbalance of energy supply and demand (Newby 1984). In the brain, adenosine acts as an inhibitory neuromodulator, which is released under conditions of neuronal activity and reduces this activity by inhibition of transmitter release and postsynaptic hyperpolarisation. Brain damage, e.g., by stroke, ischemia, and seizures leads to a pronounced increase in extracellular adenosine (for review see Rudolphi and Schubert 1996) which counteracts seizure activity (Dragunow 1988) and promotes neuronal survival (Deckert and Gleiter 1994;Picano and Abbracchio 1998;Dux et al. 1990).In addition to its role as an endogenous anticonvulsant and neuroprotective agent, adenosine is now recognized as an important regulator of sleep and wakefulness (for review see Porkka-Heiskanen 1999 (van Calker et al. 1978(van Calker et al. , 1979, but more recent findings have revealed coupling of adenosine receptors to other signaling systems including the phosphoinositol system, potassium, and calcium channels (for review see Fredholm et al. 1994;Ralevic and Burnstock 1998). Adenosine mediates neuroprotection by inhibiting presynaptically the release of several neurotransmitters including the excitatory neurotransmitter glutamate (Ribeiro 1995). Postsynaptically, adenosine increases conductances of various K ϩ -and Cl Ϫ -channels, which hyperpolarize the membrane potential and counteract a transmitter induced depolarisation with a subsequent reduction of Ca 2 ϩ -influx and stabilization of the Mg 2 ϩ blockage of NMDA receptors (Rudolphi et al. 1992a,b;Rudolphi and Schubert 1996). Most, if not all, of these actions of adenosine are mediated via the adenosine A 1 receptor, whereas the role of the other adenosine receptor subtype in neuroprotection is less clear (Schubert et al. 1997;Abbracchio and Cattabeni 1999;Heurteaux et al. 1995). Accordingly, upregulation of adenosine A 1 receptors by chronic treatment with A 1 -antagonists increases the neuroprotective effect of adenosine (Sutherland et al. 1991; Rudolphi et al. 1992a,b).Upregulation of adenosine A1-receptors is also observed after treatments that exert antidepressive effects in humans such as seizures and electroconvulsive treatment (ECT) (Newman et al. 1984;Gleiter et al. 1989;Angelatou et al..1993;Pagonopoulou et al. 1993), REM sleep deprivation (Yanik and Radulovacki 1987), and chronic treatment with carbamazepine (Daval et al. 1989;Biber et al. 1999;van Calker et al. 2000). While the upregulation by carbamazepine of adenosine A 1 receptors is readily comprehensible from carbamazepine's selective antag...

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Section: Discussionsupporting

confidence: 69%

mentioning

confidence: 99%

Interleukin-6 Enhances Expression of Adenosine A1 Receptor mRNA and Signaling in Cultured Rat Cortical Astrocytes and Brain Slices

Biber

2001

Neuropsychopharmacology

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“…Adenosine is a key neuromodulator highly implicated in the sleep-wake literature (Basheer et al 2004). Adenosine levels are known to fluctuate throughout the day, peaking during the height of the active period and then diminishing over the animal's resting period in both the hippocampus and the neostriatum (Huston et al 1996). This fluctuation in adenosine over the sleep-wake cycle has also been observed in the forebrain of animals (Porkka-Heiskanen 1997).…”

Section: Adenosine and Astrocytesmentioning

confidence: 92%

The impact of sleep loss on hippocampal function

2013

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Hippocampal cellular and molecular processes critical for memory consolidation are affected by the amount and quality of sleep attained. Questions remain with regard to how sleep enhances memory, what parameters of sleep after learning are optimal for memory consolidation, and what underlying hippocampal molecular players are targeted by sleep deprivation to impair memory consolidation and plasticity. In this review, we address these topics with a focus on the detrimental effects of post-learning sleep deprivation on memory consolidation. Obtaining adequate sleep is challenging in a society that values "work around the clock." Therefore, the development of interventions to combat the negative cognitive effects of sleep deprivation is key. However, there are a limited number of therapeutics that are able to enhance cognition in the face of insufficient sleep. The identification of molecular pathways implicated in the deleterious effects of sleep deprivation on memory could potentially yield new targets for the development of more effective drugs.

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“…Another important link between glutamate-mediated sustained depolarizations and adenosine is the sleep-wake cycle. In the cerebral cortex, levels of adenosine increase during wakefulness and during sleep deprivation [22,71]. Blocking the A1 receptor or blockade of the astrocytic release of ATP prevents cognitive deficits resulting from sleep deprivation [67].…”

Section: (Iii) A1 Antagonist Cptmentioning

confidence: 99%

Contribution of extrasynapticN-methyl-d-aspartate and adenosine A1 receptors in the generation of dendritic glutamate-mediated plateau potentials

Oikonomou

Singh

Rich

et al. 2015

Phil. Trans. R. Soc. B

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One contribution of 16 to a discussion meeting issue 'Release of chemical transmitters from cell bodies and dendrites of nerve cells'. Thin basal dendrites can strongly influence neuronal output via generation of dendritic spikes. It was recently postulated that glial processes actively support dendritic spikes by either ceasing glutamate uptake or by actively releasing glutamate and adenosine triphosphate (ATP). We used calcium imaging to study the role of NR2C/D-containing N-methyl-D-aspartate (NMDA) receptors and adenosine A1 receptors in the generation of dendritic NMDA spikes and plateau potentials in basal dendrites of layer 5 pyramidal neurons in the mouse prefrontal cortex. We found that NR2C/D glutamate receptor subunits contribute to the amplitude of synaptically evoked NMDA spikes. Dendritic calcium signals associated with glutamate-evoked dendritic plateau potentials were significantly shortened upon application of the NR2C/D receptor antagonist PPDA, suggesting that NR2C/D receptors prolong the duration of calcium influx during dendritic spiking. In contrast to NR2C/D receptors, adenosine A1 receptors act to abbreviate dendritic and somatic signals via the activation of dendritic K þ current. This current is characterized as a slow-activating outward-rectifying voltage-and adenosine-gated current, insensitive to 4-aminopyridine but sensitive to TEA. Our data support the hypothesis that the release of glutamate and ATP from neurons or glia contribute to initiation, maintenance and termination of local dendritic glutamate-mediated regenerative potentials.

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Extracellular adenosine levels in neostriatum and hippocampus during rest and activity periods of rats

Cited by 167 publications

References 41 publications

Interleukin-6 Enhances Expression of Adenosine A1 Receptor mRNA and Signaling in Cultured Rat Cortical Astrocytes and Brain Slices

Interleukin-6 Enhances Expression of Adenosine A1 Receptor mRNA and Signaling in Cultured Rat Cortical Astrocytes and Brain Slices

The impact of sleep loss on hippocampal function

Contribution of extrasynapticN-methyl-d-aspartate and adenosine A1 receptors in the generation of dendritic glutamate-mediated plateau potentials

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