Potent effect of interleukin-1β to evoke ATP and adenosine release from rat hippocampal slices

Sperlágh, Beáta; Baranyi, Mária; Haskó, György; Vizi, E. Sylvester

doi:10.1016/j.jneuroim.2004.02.004

Cited by 47 publications

(23 citation statements)

References 49 publications

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“…The measuring technique would have to be (1) sensitive enough to record changes in extracellular adenosine induced by physiological stimulation, (2) able to record locally within discrete dendritic domains, and (3) equipped with sufficient temporal resolution to resolve changes likely occurring during the minutes-long consolidation phase of LTP. Conventional extracellular purine assays, generally requiring collection of slice superfusate, lack the sensitivity, spatial resolution, or temporal resolution to meet such demands (Sperlagh et al, 1997(Sperlagh et al, , 2004Broad et al, 2000). Work now in progress is testing the possibility that recently developed voltametric enzyme biosensors (Dale et al, 2000;Pearson et al, 2001;Llaudet et al, 2003) might be able to satisfy the above criteria.…”

Section: Discussionmentioning

confidence: 99%

Long-Term Potentiation Is Impaired in Middle-Aged Rats: Regional Specificity and Reversal by Adenosine Receptor Antagonists

Rex¹,

Kramár²,

Colgin³

et al. 2005

J. Neurosci.

126

106

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Memory loss in humans begins early in adult life and progresses thereafter. It is not known whether these losses reflect the failure of cellular processes that encode memory or disturbances in events that retrieve it. Here, we report that impairments in hippocampal long-term potentiation (LTP), a form of synaptic plasticity associated with memory, are present by middle age in rats but only in select portions of pyramidal cell dendritic trees. Specifically, LTP induced with theta-burst stimulation in basal dendrites of hippocampal field CA1 decayed rapidly in slices prepared from 7-to 10-month-old rats but not in slices from young adults. There were no evident age-related differences in LTP in the apical dendrites. Both the adenosine A 1 receptor antagonist 8-cyclopentyl-1,3-dipropylxanthine and a positive AMPA receptor modulator (ampakine) offset age-related LTP deficits. Adenosine produced greater depression of synaptic responses in middle-aged versus young adult slices and in basal versus apical dendrites. These results were not associated with variations in A 1 receptor densities and may instead reflect regional and age-related differences in adenosine clearance. Pertinent to this, brief applications of A 1 receptor antagonists immediately after theta stimulation fully restored LTP in middle-aged rats. We hypothesize that the build-up of extracellular adenosine during theta activity persists into the postinduction period in the basal dendrites of middle-aged slices and thereby activates the A 1 receptor-dependent LTP reversal effect. Regardless of the underlying mechanism, the present results provide a candidate explanation for memory losses during normal aging and indicate that, with regard to plasticity, different segments of pyramidal neurons age at different rates.

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Section: Discussionmentioning

confidence: 99%

Long-Term Potentiation Is Impaired in Middle-Aged Rats: Regional Specificity and Reversal by Adenosine Receptor Antagonists

Rex¹,

Kramár²,

Colgin³

et al. 2005

J. Neurosci.

126

106

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“…Addition of A 3 R antagonist alone inhibited LPS-induced cytokine responses in both nonactivated and activated microglia. Because no exogenous adenosine was added, the inhibitory effects are most likely attributable to endogenously produced extracellular adenosine in response to LPS (25)(26)(27) and demonstrate that A 3 R-mediated signaling indeed counteracts adenosine-mediated inhibitory signaling. When A 2A R agonists were added in combination with A 3 R antagonists, inhibition was maximal in both nonactivated and activated microglia, confirming this idea.…”

Section: Important Roles For a 2a R As Well As For A 3 Rmentioning

confidence: 94%

Differential Expression of Adenosine A3 Receptors Controls Adenosine A2A Receptor-Mediated Inhibition of TLR Responses in Microglia

Putten¹,

Zuiderwijk‐Sick²,

Straalen³

et al. 2009

The Journal of Immunology

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Microglia activation is a prominent feature in many neuroinflammatory disorders. Unrestrained activation can generate a chronic inflammatory environment that might lead to neurodegeneration and autoimmunity. Extracellular adenosine modulates cellular activation through adenosine receptor (ADORA)-mediated signaling. There are four ADORA subtypes that can either increase (A2A and A2B receptors) or decrease (A1 and A3 receptors) intracellular cyclic AMP levels. The expression pattern of the subtypes thus orchestrates the cellular response to extracellular adenosine. We have investigated the expression of ADORA subtypes in unstimulated and TLR-activated primary rhesus monkey microglia. Activation induced an up-regulation of A2A and a down-regulation of A3 receptor (A3R) levels. The altered ADORA-expression pattern sensitized microglia to A2A receptor (A2AR)-mediated inhibition of subsequent TLR-induced cytokine responses. By using combinations of subtype-specific agonists and antagonists, we revealed that in unstimulated microglia, A2AR-mediated inhibitory signaling was effectively counteracted by A3R-mediated signaling. In activated microglia, the decrease in A3R-mediated signaling sensitized them to A2AR-mediated inhibitory signaling. We report a differential, activation state-specific expression of ADORA in microglia and uncover a role for A3R as dynamically regulated suppressors of A2AR-mediated inhibition of TLR-induced responses. This would suggest exploration of combinations of A2AR agonists and A3R antagonists to dampen microglial activation during chronic neuroinflammatory conditions.

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“…Tumor necrosis factor-␣ (TNF-␣) rapidly up-regulates membrane expression of neuronal AMPA receptors (Beattie et al, 2002) and increases AMPA conductance . TNF-␣ also enhances neuroexcitability in response to glutamate (Emch et al, 2001), and IL-1␤ induces the release of the neuroexcitant ATP via an NMDA-mediated mechanism (Sperlá gh et al, 2004). In addition, proinflammatory cytokines can induce the production of a variety of neuroexcitatory substances, including nitric oxide, prostaglandins, and reactive oxygen species (Watkins et al, 1999;Samad et al, 2001 (Meller et al, 1994;Reeve et al, 2000;Kehl et al, 2004).…”

Section: What Is the Impact Of The Central Immunementioning

confidence: 99%

Exploring the Neuroimmunopharmacology of Opioids: An Integrative Review of Mechanisms of Central Immune Signaling and Their Implications for Opioid Analgesia

Hutchinson

Shavit

Grace³

et al. 2011

Pharmacol Rev

343

315

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Potent effect of interleukin-1β to evoke ATP and adenosine release from rat hippocampal slices

Cited by 47 publications

References 49 publications

Long-Term Potentiation Is Impaired in Middle-Aged Rats: Regional Specificity and Reversal by Adenosine Receptor Antagonists

Long-Term Potentiation Is Impaired in Middle-Aged Rats: Regional Specificity and Reversal by Adenosine Receptor Antagonists

Differential Expression of Adenosine A3 Receptors Controls Adenosine A2A Receptor-Mediated Inhibition of TLR Responses in Microglia

Exploring the Neuroimmunopharmacology of Opioids: An Integrative Review of Mechanisms of Central Immune Signaling and Their Implications for Opioid Analgesia

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