Potentiation of the action of adenosine on cerebral cortical neurones by the tricyclic antidepressants

Phillis, John W.

doi:10.1111/j.1476-5381.1984.tb16521.x

Cited by 39 publications

(11 citation statements)

References 41 publications

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“…There is some evidence that adenosine is involved in the actions of antidepressants. These agents potentiated the depressant actions of adenosine on rat cortical slices (Phillis, 1984). The effect of the antidepressant drugs amitriptyline (AMI) and CTP on rat prefrontal cortex was blocked by the adenosine A 1 receptor antagonist, 8-cyclopentyltheophylline (Golembiowska and Dziubina, 2001).…”

Section: Discussionmentioning

confidence: 99%

Mechanism of inhibitory effect of citalopram on isolated guinea‐pig atria in relation to adenosine receptor

Pousti

Deemyad

Malihi

2004

Human Psychopharmacology

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The effect of citalopram (CTP), a selective serotonin reuptake inhibitor antidepressant was studied on the rate and force of contractions of isolated guinea-pig atria. CTP (2-32 microg/ml) caused a dose-dependent decrease in the contractile force (7%-62%) and in the rate of contractions (11%-72%). These negative inotropic and chronotropic effects of CTP (8 microg/ml) were not prevented by atropine (1 microg/ml) and 3,7 dimethyl-1-propargylxanthine (DMPX; 1.5 microg/ml), an adenosine A(2) receptor antagonist, but 1,3 dipropargyl-8-cyclopentylxanthine (DPCPX; 12 microg/ml), a specific adenosine A(1) receptor antagonist significantly blocked these effects (p < 0.001) and theophylline (30 microg/ml) a non-selective adenosine A(1)/A(2A) receptor antagonist also prevented the inotropic and chronotropic effects of CTP. These results suggest that the negative inotropic and chronotropic effect of CTP on isolated guinea-pig atria is probably mediated through an inhibition of the uptake of adenosine or the A(1) receptor mechanism.

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Section: Discussionmentioning

confidence: 99%

Mechanism of inhibitory effect of citalopram on isolated guinea‐pig atria in relation to adenosine receptor

Pousti

Deemyad

Malihi

2004

Human Psychopharmacology

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“…Similarly, tricyclic antidepressants (TCAs) increased inhibition of cortical neuron firing and potentiated the effects of adenosine on cortical neurons (Stone and Taylor, 1978; Phillis, 1984). Aggressive behavior induced by clonidine was overcome by adenosine receptor antagonism (Ushijima et al, 1989).…”

Section: The Purinergic System: Neurobiological Findings In Mood Dmentioning

confidence: 99%

Purinergic system dysfunction in mood disorders: a key target for developing improved therapeutics

Ortiz

Ulrich

Zarate

et al. 2015

Progress in Neuro-Psychopharmacology and Biological Psychiatry

103

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Uric acid and purines (such as adenosine) regulate mood, sleep, activity, appetite, cognition, memory, convulsive threshold, social interaction, drive, and impulsivity. A link between purinergic dysfunction and mood disorders was first proposed a century ago. Interestingly, a recent nationwide population-based study showed elevated risk of gout in subjects with bipolar disorder (BD), and a recent meta-analysis and systematic review of placebo-controlled trials of adjuvant purinergic modulators confirmed their benefits in bipolar mania. Uric acid may modulate energy and activity levels, with higher levels associated with higher energy and BD spectrum. Several recent genetic studies suggest that the purinergic system particularly the modulation of P1 and P2 receptor subtypes—plays a role in mood disorders, lending credence to this model. Nucleotide concentrations can be measured using brain spectroscopy, and ligands for in vivo positron emission tomography (PET) imaging of adenosine (P1) receptors have been developed, thus allowing potential target engagement studies. This review discusses the key role of the purinergic system in the pathophysiology of mood disorders. Focusing on this promising therapeutic target may lead to the development of therapies with antidepressant, mood stabilization, and cognitive effects.

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“…Interestingly, classical tricyclic antidepressants such as nortriptiline, chlorimipramine or desipramine can bind to adenosine receptors [153] and dose-dependently reduce the activity of ectonucleotidases in cortical nerve terminals [154], a key controller of the extracellular formation of adenosine from released adenine nucleotides [56]. Accordingly, these tricyclic antidepressants modify the outflow of adenosine from cortical cups [155][156] and the glucose and ATP levels in healthy volunteers [157][158][159][160].…”

Section: Adenosine a 2a Receptors And Depressionmentioning

confidence: 99%

Potential Therapeutic Interest of Adenosine A2A Receptors in Psychiatric Disorders

Cunha¹,

Ferré²,

Vaugeois³

et al. 2008

CPD

174

149

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The interest on targeting adenosine A 2A receptors in the realm of psychiatric diseases first arose based on its tight physical and functional interaction with dopamine D 2 receptors. However, the role of central A 2A receptors is now viewed as much broader than just controlling D 2 receptor function. Thus, there is currently a major interest in the ability of A 2A receptors to control synaptic plasticity at glutamatergic synapses. This is due to a combined ability of A 2A receptors to facilitate the release of glutamate and the activation of NMDA. Therefore, A 2A receptors are now conceived as a normalizing device promoting adequate adaptive responses in neuronal circuits, a role similar to that fulfilled, in essence, by dopamine. This makes A 2A receptors a particularly attractive target to manage psychiatric disorders since adenosine may act as go-between glutamate and dopamine, two of the key players in mood processing. Furthermore, A 2A receptors also control glia function and brain metabolic adaptation, two other emerging mechanisms to understand abnormal processing of mood, and A 2A receptors are an important player in controlling the demise of neurodegeneration, considered an amplificatory loop in psychiatric disorders. Current data only provide an indirect confirmation of this putative role of A 2A receptors, based on the effects of caffeine (an antagonist of both A 1 and A 2A receptors) in psychiatric disorders. However, the introduction of A 2A receptors in clinics as antiparkinsonian agents is hoped to bolster our knowledge on the role of A 2A receptors in mood disorders in the near future.

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Potentiation of the action of adenosine on cerebral cortical neurones by the tricyclic antidepressants

Cited by 39 publications

References 41 publications

Mechanism of inhibitory effect of citalopram on isolated guinea‐pig atria in relation to adenosine receptor

Mechanism of inhibitory effect of citalopram on isolated guinea‐pig atria in relation to adenosine receptor

Purinergic system dysfunction in mood disorders: a key target for developing improved therapeutics

Potential Therapeutic Interest of Adenosine A2A Receptors in Psychiatric Disorders

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