15 research outputs found
Bird community in a forest patch isolated by the urban matrix at the Sinos River basin, Rio Grande do Sul state, Brazil, with comments on the possible local defaunation
Seasonal influence on the essential oil production of Nectandra megapotamica (Spreng.) Mez
Raptor assemblages in grasslands of Southern Brazil: species richness and abundance and the influence of the survey method
Depressive symptoms are associated with tumor necrosis factor alpha in systemic lupus erythematosus
Electroconvulsive therapy: a novel hypothesis for the involvement of purinergic signalling
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