The aim of this research was to follow parallelly the clinical status of a patient and the dynamics of the serotonin transporter (SERT), a likely player in the effect of electroconvulsive treatment (ECT), a powerful tool against deep depression. A patient affected by major depression with catatonic features, not responding to pharmacological therapy, underwent ECT. Evaluations of the binding of labelled paroxetine to venous blood platelet SERT were parallel to the assessments of clinical improvements. The density of platelet SERT, starting from a low level before ECT, displayed an initial steep increase peaking the day after the third electroconvulsive session (5 days after the start of ECT). This was followed by a rapid decrease, which seemed to precede the process of clinical recovery. These results were found in a case of unavoidable ECT treatment. If generalizable, they suggest interesting ideas about the still mysterious mechanism of ECT antidepressant action.