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Cerebral Cortex Advance Access originally published online on June 7, 2007
Cerebral Cortex 2008 18(2):424-432; doi:10.1093/cercor/bhm077
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© The Author 2007. Published by Oxford University Press. All rights reserved. For permissions, please e-mail: journals.permissions@oxfordjournals.org

Developmental Downregulation of Excitatory GABAergic Transmission in Neocortical Layer I via Presynaptic Adenosine A1 Receptors

Knut Kirmse, Anton Dvorzhak1, Rosemarie Grantyn and Sergei Kirischuk

Institute of Neurophysiology, Johannes-Mueller-Center of Physiology, Charité-University-Medicine Berlin, Tucholskystr. 2, 10117 Berlin, Germany, 1 Permanent address: Department of Fundamental and Applied Physiology, Russian States Medical University, Ostrovitjanova 1, 117997 Moscow, Russia

Address correspondence to Dr Sergei Kirischuk, Institute of Neurophysiology, Johannes-Mueller-Center of Physiology, Charité-University-Medicine Berlin, Tucholskystr. 2, 10117 Berlin, Germany. Email: sergei.kirischuk{at}charite.de.

Layer I of the developing cortex contains a dense GABAergic fiber plexus. These fibers provide excitatory inputs to Cajal-Retzius (CR) cells, the early born neurons in layer I. CR cells possess an extensive axonal projection and form synaptic contacts with excitatory, presumably pyramidal, neurons before birth. Interestingly, activity of CR cells declines during the first postnatal week, but mechanism(s) underlying this phenomenon is not yet known. Here we recorded inhibitory postsynaptic currents (IPSCs) in CR cells at postnatal day (P) 1–2 and P5–7. Blockade of adenosine A1 receptors (A1Rs) increased the amplitude of evoked IPSCs (eIPSCs) and decreased paired-pulse ratio at P5–7 but not at P1–2. A1R activation decreased the mean eIPSC amplitude at P5–7, but failed to affect eIPSCs at P1–2. Ecto-adenosine triphosphatase (ATPase) inhibition completely abolished the A1R-mediated effects suggesting that extracellular ATP is the main source of adenosine. Because A1R blockade did not affect the median miniature IPSC amplitude, our results demonstrate that adenosine reduces {gamma}-aminiobutyric acid (GABA) release probability via presynaptic A1Rs at P5–7. As neuronal activity in layer I can depolarize pyramidal neurons influencing thereby glutamatergic synaptogenesis in the lower cortical layers, postnatal weakening of GABAergic transmission by adenosinergic system might reflect a developmental downregulation of this excitatory drive when glutamatergic synapses are formed.

Key Words: ATP release • ecto-ATPase • GABAB • GPCR • short-term plasticity


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