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Abstract
It is established that purinergic signaling can shape a wide range of physiological functions, including neurotransmission and neuromodulation. The purinergic system may play a role in the pathophysiology of mood disorders, influencing neurotransmitter systems and hormonal pathways of the hypothalamic-pituitary-adrenal axis. Treatment with mood stabilizers and antidepressants can lead to changes in purinergic signaling. In this overview, we describe the biological background on the possible link between the purinergic system and depression, possibly involving changes in adenosine- and ATP-mediated signaling at P1 and P2 receptors, respectively. Furthermore, evidence on the possible antidepressive effects of non-selective adenosine antagonist caffeine and other purinergic modulators is reviewed. In particular, A2A and P2X7 receptors have been identified as potential targets for depression treatment. Preclinical studies highlight that both selective A2A and P2X7 antagonists may have antidepressant effects and potentiate responses to antidepressant treatments. Consistently, recent studies feature the possible role of the purinergic system peripheral metabolites as possible biomarkers of depression. In particular, variations of serum uric acid, as the end product of purinergic metabolism, have been found in depression. Although several open questions remain, the purinergic system represents a promising research area for insights into the molecular basis of depression.
Highlights
The purine nucleoside adenosine was identified in 1929 by Drury and Szent-György [1], who described the physiological activity of adenine compounds in the mammalian heart
We describe the biological background of the possible link between the purinergic system and depression, summarizing epidemiological and preclinical evidence of the possible effects of caffeine and other purinergic modulators, as well as the role of relevant biomarkers in depression
Purinergic signaling may play a role in the pathophysiology of depression involving the inhibition of A1 and the activation of A2A receptors, as well as P2 receptors
Summary
The purine nucleoside adenosine was identified in 1929 by Drury and Szent-György [1], who described the physiological activity of adenine compounds in the mammalian heart. Components of purinergic signaling and related metabolism of adenosine may be implicated in depressive disorders In this overview, we describe the biological background of the possible link between the purinergic system and depression, summarizing epidemiological and preclinical evidence of the possible effects of caffeine and other purinergic modulators, as well as the role of relevant biomarkers in depression. The possible role of the purinergic system and, in particular, of adenosine and P1 receptors in depression is mainly derived from studies on the association between caffeine consumption and related mood changes [22,23]. A large cohort study conducted in Korea on 80,173 individuals showed that regular and moderate caffeine intake was likely to reduce suicide risk and depression in women, despite higher consumption levels associated to worse outcomes [29]. J-shaped association of caffeine with the risk of suicide [30]
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