Impact of electroconvulsive therapy on the adenosine A ₁ receptor in the human brain: A PET study in depressive patients

Ziel/Aim Major depressive disorder (MDD) severely influences life quality and is one of the major causes of suicide. Besides pharmaco- and psychotherapy, sleep deprivation and electroconvulsive therapy (ECT) are effective treatments. Both are associated with an enhancement of adenosine levels, which in turn likely influence adenosinergic receptor expression, ultimately resulting in therapeutic efficacy. The current study investigates if changes of the adenosine A₁ receptor (A₁AR) could account for anti-depressive properties of ECT in patients with MDD.

Methodik/Methods In total, 14 depressive patients were investigated twice by means of specific A₁AR-PET. The first scan served as baseline whereas the second was performed after ECT treatment (10.4 ± 1.2 sessions, last ECT 5.7 ± 2.7 days before the second scan). Regional A₁AR receptor availability was determined via an equilibrium approach based on a metabolite-corrected plasma input function and further analyzed by a mixed model analysis of variance. Additionally, all patients underwent neuropsychological testing to correlate clinical outcome parameters with molecular changes of A₁AR.

Ergebnisse/Results Cerebral A₁AR expression before and after ECT was stable in grey matter (F_(1,13) = 0.026; p = 0.88) and responders/non-responders behaved the same (‘responder/non-responder’: p = 0.31, ‘region × scan session × responder/non-responder’: p = 0.16). There was no correlation between changes in clinical outcome parameters and regional A₁AR densities although individual patients showed striking alterations in A₁AR expression after ECT treatment.

Schlussfolgerungen/Conclusions In the investigated sample ECT did neither lead to consistent changes in A₁AR expression, nor did clinical outcome after ECT correlate with alterations in A₁AR availabilities. In conclusion, the results of the present study imply that clinical effects of ECT cannot be explained by long-lasting changes of the cerebral A₁AR. This does, however, not rule out that other routes of purinergic signaling are involved in ECT efficacy.