Electroconvulsive therapy: a novel hypothesis for the involvement of purinergic signalling |
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Authors: | Ahmed-Ramadan Sadek Gillian E Knight Geoffrey Burnstock |
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Institution: | (1) Wessex Neurological Centre, Southampton University Hospitals NHS Trust, Tremona Road, Southampton, SO16 6YD, UK;(2) Division of Clinical Neurosciences, School of Medicine, University of Southampton, Tremona Road, Southampton, SO16 6YD, UK;(3) Autonomic Neuroscience Centre, University College Medical School, Royal Free Campus, Rowland Hill Street, London, NW3 2PF, UK |
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Abstract: | It is proposed that ATP is released from both neurons and glia during electroconvulsive therapy (ECT) and that this leads
to reduction of depressive behaviour via complex stimulation of neurons and glia directly via P2X and P2Y receptors and also
via P1 receptors after extracellular breakdown of ATP to adenosine. In particular, A1 adenosine receptors inhibit release of excitatory transmitters, and A2A and P2Y receptors may modulate the release of dopamine. Sequential ECT may lead to changes in purinoceptor expression in
mesolimbic and mesocortical regions of the brain implicated in depression and other mood disorders. In particular, increased
expression of P2X7 receptors on glial cells would lead to increased release of cytokines, chemokines and neurotrophins. In
summary, we suggest that ATP release following ECT involves neurons, glial cells and neuron–glial interactions acting via
both P2 and after breakdown to adenosine via P1 receptors. We suggest that ecto-nucleotidase inhibitors (increasing available
amounts of ATP) and purinoceptor agonists may enhance the anti-depressive effect of ECT. |
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Keywords: | ATP Depression Electroconvulsive therapy Mood Puringeric signalling |
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