P2Y Receptors in Synaptic Transmission and Plasticity: Therapeutic Potential in Cognitive Dysfunction

ATP released from neurons and astrocytes during neuronal activity or under pathophysiological circumstances is able to influence information flow in neuronal circuits by activation of ionotropic P2X and metabotropic P2Y receptors and subsequent modulation of cellular excitability, synaptic strength,...

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Main Authors: Segundo J. Guzman, Zoltan Gerevich
Format: Article
Language:English
Published: Wiley 2016-01-01
Series:Neural Plasticity
Online Access:http://dx.doi.org/10.1155/2016/1207393
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author Segundo J. Guzman
Zoltan Gerevich
author_facet Segundo J. Guzman
Zoltan Gerevich
author_sort Segundo J. Guzman
collection DOAJ
description ATP released from neurons and astrocytes during neuronal activity or under pathophysiological circumstances is able to influence information flow in neuronal circuits by activation of ionotropic P2X and metabotropic P2Y receptors and subsequent modulation of cellular excitability, synaptic strength, and plasticity. In the present paper we review cellular and network effects of P2Y receptors in the brain. We show that P2Y receptors inhibit the release of neurotransmitters, modulate voltage- and ligand-gated ion channels, and differentially influence the induction of synaptic plasticity in the prefrontal cortex, hippocampus, and cerebellum. The findings discussed here may explain how P2Y1 receptor activation during brain injury, hypoxia, inflammation, schizophrenia, or Alzheimer’s disease leads to an impairment of cognitive processes. Hence, it is suggested that the blockade of P2Y1 receptors may have therapeutic potential against cognitive disturbances in these states.
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spelling doaj-art-5120b6f7e91241259774d53e8f786f622025-02-03T01:12:33ZengWileyNeural Plasticity2090-59041687-54432016-01-01201610.1155/2016/12073931207393P2Y Receptors in Synaptic Transmission and Plasticity: Therapeutic Potential in Cognitive DysfunctionSegundo J. Guzman0Zoltan Gerevich1Institute of Science and Technology Austria (IST Austria), Am Campus 1, 3400 Klosterneuburg, AustriaInstitute of Neurophysiology, Charité-Universitätsmedizin Berlin, Charitéplatz 1, 10117 Berlin, GermanyATP released from neurons and astrocytes during neuronal activity or under pathophysiological circumstances is able to influence information flow in neuronal circuits by activation of ionotropic P2X and metabotropic P2Y receptors and subsequent modulation of cellular excitability, synaptic strength, and plasticity. In the present paper we review cellular and network effects of P2Y receptors in the brain. We show that P2Y receptors inhibit the release of neurotransmitters, modulate voltage- and ligand-gated ion channels, and differentially influence the induction of synaptic plasticity in the prefrontal cortex, hippocampus, and cerebellum. The findings discussed here may explain how P2Y1 receptor activation during brain injury, hypoxia, inflammation, schizophrenia, or Alzheimer’s disease leads to an impairment of cognitive processes. Hence, it is suggested that the blockade of P2Y1 receptors may have therapeutic potential against cognitive disturbances in these states.http://dx.doi.org/10.1155/2016/1207393
spellingShingle Segundo J. Guzman
Zoltan Gerevich
P2Y Receptors in Synaptic Transmission and Plasticity: Therapeutic Potential in Cognitive Dysfunction
Neural Plasticity
title P2Y Receptors in Synaptic Transmission and Plasticity: Therapeutic Potential in Cognitive Dysfunction
title_full P2Y Receptors in Synaptic Transmission and Plasticity: Therapeutic Potential in Cognitive Dysfunction
title_fullStr P2Y Receptors in Synaptic Transmission and Plasticity: Therapeutic Potential in Cognitive Dysfunction
title_full_unstemmed P2Y Receptors in Synaptic Transmission and Plasticity: Therapeutic Potential in Cognitive Dysfunction
title_short P2Y Receptors in Synaptic Transmission and Plasticity: Therapeutic Potential in Cognitive Dysfunction
title_sort p2y receptors in synaptic transmission and plasticity therapeutic potential in cognitive dysfunction
url http://dx.doi.org/10.1155/2016/1207393
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