10
views
0
recommends
+1 Recommend
0 collections
    0
    shares
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      Adenosine A 2A Receptors Control Glutamatergic Synaptic Plasticity in Fast Spiking Interneurons of the Prefrontal Cortex

      research-article

      Read this article at

      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Adenosine A 2A receptors (A 2AR) are activated upon increased synaptic activity to assist in the implementation of long-term plastic changes at synapses. While it is reported that A 2AR are involved in the control of prefrontal cortex (PFC)-dependent behavior such as working memory, reversal learning and effort-based decision making, it is not known whether A 2AR control glutamatergic synapse plasticity within the medial PFC (mPFC). To elucidate that, we tested whether A 2AR blockade affects long-term plasticity (LTP) of excitatory post-synaptic potentials in pyramidal neurons and fast spiking (FS) interneurons in layer 5 of the mPFC and of population spikes. Our results show that A 2AR are enriched at mPFC synapses, where their blockade reversed the direction of plasticity at excitatory synapses onto layer 5 FS interneurons from LTP to long-term depression, while their blockade had no effect on the induction of LTP at excitatory synapses onto layer 5 pyramidal neurons. At the network level, extracellularly induced LTP of population spikes was reduced by A 2AR blockade. The interneuron-specificity of A 2AR in controlling glutamatergic synapse LTP may ensure that during periods of high synaptic activity, a proper excitation/inhibition balance is maintained within the mPFC.

          Related collections

          Most cited references63

          • Record: found
          • Abstract: found
          • Article: not found

          Interneurons of the neocortical inhibitory system.

          Mammals adapt to a rapidly changing world because of the sophisticated cognitive functions that are supported by the neocortex. The neocortex, which forms almost 80% of the human brain, seems to have arisen from repeated duplication of a stereotypical microcircuit template with subtle specializations for different brain regions and species. The quest to unravel the blueprint of this template started more than a century ago and has revealed an immensely intricate design. The largest obstacle is the daunting variety of inhibitory interneurons that are found in the circuit. This review focuses on the organizing principles that govern the diversity of inhibitory interneurons and their circuits.
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            The role of medial prefrontal cortex in memory and decision making.

            Some have claimed that the medial prefrontal cortex (mPFC) mediates decision making. Others suggest mPFC is selectively involved in the retrieval of remote long-term memory. Yet others suggests mPFC supports memory and consolidation on time scales ranging from seconds to days. How can all these roles be reconciled? We propose that the function of the mPFC is to learn associations between context, locations, events, and corresponding adaptive responses, particularly emotional responses. Thus, the ubiquitous involvement of mPFC in both memory and decision making may be due to the fact that almost all such tasks entail the ability to recall the best action or emotional response to specific events in a particular place and time. An interaction between multiple memory systems may explain the changing importance of mPFC to different types of memories over time. In particular, mPFC likely relies on the hippocampus to support rapid learning and memory consolidation. Copyright © 2012 Elsevier Inc. All rights reserved.
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              Enforcement of temporal fidelity in pyramidal cells by somatic feed-forward inhibition.

              The temporal resolution of neuronal integration depends on the time window within which excitatory inputs summate to reach the threshold for spike generation. Here, we show that in rat hippocampal pyramidal cells this window is very narrow (less than 2 milliseconds). This narrowness results from the short delay with which disynaptic feed-forward inhibition follows monosynaptic excitation. Simultaneous somatic and dendritic recordings indicate that feed-forward inhibition is much stronger in the soma than in the dendrites, resulting in a broader integration window in the latter compartment. Thus, the subcellular partitioning of feed-forward inhibition enforces precise coincidence detection in the soma, while allowing dendrites to sum incoming activity over broader time windows.
                Bookmark

                Author and article information

                Contributors
                Journal
                Front Pharmacol
                Front Pharmacol
                Front. Pharmacol.
                Frontiers in Pharmacology
                Frontiers Media S.A.
                1663-9812
                20 March 2018
                2018
                : 9
                : 133
                Affiliations
                [1] 1Department of Integrative Neurophysiology, Center for Neurogenomics and Cognitive Research, VU University , Amsterdam, Netherlands
                [2] 2Center for Neuroscience and Cell Biology, University of Coimbra , Coimbra, Portugal
                [3] 3Faculty of Medicine, University of Coimbra , Coimbra, Portugal
                Author notes

                Edited by: Francisco Ciruela, Universitat de Barcelona, Spain

                Reviewed by: Elena Martín-García, Pompeu Fabra University, Spain; Carl Richard Lupica, National Institute on Drug Abuse (NIH), United States

                *Correspondence: Samira G. Ferreira, carsamira@ 123456gmail.com

                This article was submitted to Experimental Pharmacology and Drug Discovery, a section of the journal Frontiers in Pharmacology

                Article
                10.3389/fphar.2018.00133
                5869254
                29615897
                0a2075da-909a-4cbb-bcbb-2b9c6c602bc2
                Copyright © 2018 Kerkhofs, Canas, Timmerman, Heistek, Real, Xavier, Cunha, Mansvelder and Ferreira.

                This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

                History
                : 02 September 2017
                : 07 February 2018
                Page count
                Figures: 5, Tables: 0, Equations: 0, References: 71, Pages: 12, Words: 0
                Funding
                Funded by: Horizon 2020 Framework Programme 10.13039/100010661
                Award ID: agreement no. 604102 “Human Brain Project”
                Funded by: Seventh Framework Programme 10.13039/100011102
                Award ID: EU MSCA-ITN CognitionNet FP7-PEOPLE-2013-ITN 607508
                Funded by: Fundação para a Ciência e a Tecnologia 10.13039/501100001871
                Award ID: POCI-01-0145-FEDER-007440
                Award ID: PTDC/NEU-NMC/4154/2016
                Categories
                Pharmacology
                Original Research

                Pharmacology & Pharmaceutical medicine
                a2a receptor,prefrontal cortex (pfc),synaptic plasticity,fast-spiking interneurons,adenosine,ltp and ltd,electrophysiology

                Comments

                Comment on this article