Modulation of gamma oscillations by endogenous adenosine through A1 and A2A receptors in the mouse hippocampus

Pietersen, Alexander N.J.; Lancaster, D.M.; Patel, Nisha; Hamilton, James B.; Vreugdenhil, Martin

doi:10.1016/j.neuropharm.2008.10.001

Cited by 42 publications

(33 citation statements)

References 37 publications

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“…A modulatory role for adenosine A 1 receptors in cortical oscillations has been described previously (Pietersen et al, 2009), including for oscillations dependent upon release of adenosine from astrocytes (Fellin et al, 2009). …”

Section: Purinergic Regulation Of Mglur-dependent Oscillationsmentioning

confidence: 89%

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: Purinergic Regulation Of Mglur-dependent Oscillationsmentioning

confidence: 89%

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

2015

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“…Caffeine, which is an adenosine receptor antagonist, exerts reinforcing effects that are ADORA2A-dependent (Casta et al, 2006) and are associated with downstream phosphorylation of DARPP-32 (Hsu et al, 2009). The ADORA2A-dependent promotion of the 'down state' is further supported by studies finding gamma oscillation strength is opposed by A(2A) receptors (Pietersen et al, 2009). Many of the other novel genes described above are presently distinguished merely as being enriched in terminally differentiated cells, however, the wider literature suggests clues on their roles in cell differentiation migration and connectivity, and hence, information-processing functions of MSNs.…”

Section: Hypothesis Development For Novel Striatonigraland Striatopalmentioning

confidence: 93%

Neurogenetics and Pharmacology of Learning, Motivation, and Cognition

Frank

Fossella

2010

Neuropsychopharmacol

171

167

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Many of the individual differences in cognition, motivation, and learningFand the disruption of these processes in neurological conditionsFare influenced by genetic factors. We provide an integrative synthesis across human and animal studies, focusing on a recent spate of evidence implicating a role for genes controlling dopaminergic function in frontostriatal circuitry, including COMT, DARPP-32, DAT1, DRD2, and DRD4. These genetic effects are interpreted within theoretical frameworks developed in the context of the broader cognitive and computational neuroscience literature, constrained by data from pharmacological, neuroimaging, electrophysiological, and patient studies. In this framework, genes modulate the efficacy of particular neural computations, and effects of genetic variation are revealed by assays designed to be maximally sensitive to these computations. We discuss the merits and caveats of this approach and outline a number of novel candidate genes of interest for future study.

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“…In vivo and in vitro data show increased energy demand during gamma oscillations (Niessing et al, 2005) and that gamma oscillations are highly sensitive to decreases in oxygen tension (Fano et al, 2007;Huchzermeyer et al, 2008;Pietersen et al, 2009). How can we explain the step-like reduction of the gamma activity after the HFD and DC shift complex?…”

Section: Hfd and DC Shift During Hippocampal Ischemiamentioning

confidence: 99%

Changes in Hippocampal Neuronal Activity During and After Unilateral Selective Hippocampal IschemiaIn Vivo

Barth¹,

Módy²

2011

J. Neurosci.

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The hippocampal formation is one of the brain regions most sensitive to ischemic damage. However, there are no studies about changes in hippocampal neuronal activity during and after a selective unilateral hippocampal ischemia. We developed a novel unilateral cerebrovascular ischemia model in mice that selectively shuts down blood supply to the ipsilateral hippocampal formation. Using a modified version of the photothrombotic method, we stereotaxically targeted the initial ascending part of the longitudinal hippocampal artery in urethane anesthetized and rose bengal-injected mice. To block blood flow in the targeted artery, we photoactivated the rose bengal by illuminating the longitudinal hippocampal artery through an optical fiber inserted into the brain. In vivo field potential recordings in the CA1 region of the hippocampus before, during and after the induction of ischemia demonstrated a high-frequency discharge (HFD) reaching frequencies of Ͼ300 Hz and lasting 7-24 s during the illumination consistent with a massive synchronous neuronal activity. The HFD was invariably followed by a DC voltage shift and a decreased activity at both low (30 -57 Hz)-and high (63-119 Hz)-gamma frequencies. This decrease in gamma activity lasted for the entire duration of the recordings (ϳ160 min) following ischemia. The contralateral hippocampus displayed HFDs but with different frequency spectra and without DC voltage shifts or long-lasting decreases in gamma oscillations. Our findings reveal for the first time the acute effects of unilateral hippocampal ischemia on ensemble hippocampal neuronal activities.

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Modulation of gamma oscillations by endogenous adenosine through A1 and A2A receptors in the mouse hippocampus

Cited by 42 publications

References 37 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

Neurogenetics and Pharmacology of Learning, Motivation, and Cognition

Changes in Hippocampal Neuronal Activity During and After Unilateral Selective Hippocampal IschemiaIn Vivo

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