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@ARTICLE{Poil:17818,
      author       = {Poil, S.S. and Jansen, R. and van Aerde, K. and Timmerman,
                      J. and Brussaard, A.B. and Mansvelder, H.D. and
                      Linkenkaer-Hansen, K.},
      title        = {{F}ast network oscillations in vitro exhibit a slow decay
                      of temporal auto-correlations},
      journal      = {European journal of neuroscience},
      volume       = {34},
      issn         = {0953-816X},
      address      = {Oxford [u.a.]},
      publisher    = {Blackwell},
      reportid     = {PreJuSER-17818},
      pages        = {394 - 403},
      year         = {2011},
      note         = {This work was supported by The Netherlands Organization for
                      Scientific Research (NWO) [Toptalent grant to S.-S.P.; R.J.
                      was supported by a Computational Life Sciences grant
                      (635.100.005); Innovative Research Incentive Schemes grant
                      to K. L.-H.], the Neuro-Bsik Mouse Phenomics consortium
                      (http://www.neurobsik.nl) (grant to A. B. B), the Royal
                      Netherlands Academy of Arts and Sciences (KNAW) (fellowship
                      to H. D. M.), and the Danish Research Agency (to K.L.-H.).},
      abstract     = {Ongoing neuronal oscillations in vivo exhibit non-random
                      amplitude fluctuations as reflected in a slow decay of
                      temporal auto-correlations that persist for tens of seconds.
                      Interestingly, the decay of auto-correlations is altered in
                      several brain-related disorders, including epilepsy,
                      depression and Alzheimer's disease, suggesting that the
                      temporal structure of oscillations depends on intact
                      neuronal networks in the brain. Whether structured amplitude
                      modulation occurs only in the intact brain or whether
                      isolated neuronal networks can also give rise to amplitude
                      modulation with a slow decay is not known. Here, we examined
                      the temporal structure of cholinergic fast network
                      oscillations in acute hippocampal slices. For the first
                      time, we show that a slow decay of temporal correlations can
                      emerge from synchronized activity in isolated hippocampal
                      networks from mice, and is maximal at intermediate
                      concentrations of the cholinergic agonist carbachol. Using
                      zolpidem, a positive allosteric modulator of GABA(A)
                      receptor function, we found that increased inhibition leads
                      to longer oscillation bursts and more persistent temporal
                      correlations. In addition, we asked if these findings were
                      unique for mouse hippocampus, and we therefore analysed
                      cholinergic fast network oscillations in rat prefrontal
                      cortex slices. We observed significant temporal
                      correlations, which were similar in strength to those found
                      in mouse hippocampus and human cortex. Taken together, our
                      data indicate that fast network oscillations with temporal
                      correlations can be induced in isolated networks in vitro in
                      different species and brain areas, and therefore may serve
                      as model systems to investigate how altered temporal
                      correlations in disease may be rescued with pharmacology.},
      keywords     = {Animals / Carbachol: pharmacology / Cholinergic Agonists:
                      pharmacology / Dose-Response Relationship, Drug /
                      Electrophysiology / GABA-A Receptor Agonists: pharmacology /
                      Hippocampus: anatomy $\&$ histology / Hippocampus: drug
                      effects / Hippocampus: physiology / Humans / Male / Membrane
                      Potentials: physiology / Mice / Mice, Inbred DBA / Nerve
                      Net: anatomy $\&$ histology / Nerve Net: drug effects /
                      Nerve Net: physiology / Periodicity / Prefrontal Cortex:
                      anatomy $\&$ histology / Prefrontal Cortex: drug effects /
                      Prefrontal Cortex: physiology / Pyridines: pharmacology /
                      Rats / Rats, Wistar / Cholinergic Agonists (NLM Chemicals) /
                      GABA-A Receptor Agonists (NLM Chemicals) / Pyridines (NLM
                      Chemicals) / Carbachol (NLM Chemicals) / zolpidem (NLM
                      Chemicals) / J (WoSType)},
      cin          = {INM-2},
      ddc          = {610},
      cid          = {I:(DE-Juel1)INM-2-20090406},
      pnm          = {Funktion und Dysfunktion des Nervensystems (FUEK409) /
                      89571 - Connectivity and Activity (POF2-89571)},
      pid          = {G:(DE-Juel1)FUEK409 / G:(DE-HGF)POF2-89571},
      shelfmark    = {Neurosciences},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:21692883},
      UT           = {WOS:000293350200005},
      doi          = {10.1111/j.1460-9568.2011.07748.x},
      url          = {https://juser.fz-juelich.de/record/17818},
}