Electroconvulsive therapy (ECT) is an efficacious and safe method for the treatment of
mood disorders. Its utilization is accompanied by a myriad of biochemical and cellular changes, which are far from fully understood. The present work investigates in rat serum the effects of
seizures induced by electroconvulsive shocks (ECS), an animal model of ECT, on
enzymes that hydrolyze
ATP,
ADP and
AMP to
adenosine. Two different models of ECS were used, consisting in the application of one or eight ECS sessions, and respectively named acute or chronic. Serum samples were collected at several time points after the single
shock in the acute and after the eighth and last
shock in the chronic model. A single
shock produced a sudden and short-lived inhibition of enzymatic activity (P<0.01 for
ADP and
AMP), whereas in the chronic model significant increases were noticed starting as early as 12 h after the last
shock, remaining significantly elevated until the last measurement 7 days later for
ATP and
ADP. Analysis of hydrolysis was assessed at the selected time point of 7 days in cerebrospinal fluid samples, also demonstrating a significant activation in the chronic model (P<0.0001 for
ATP and
ADP). These results support the idea that
adenosine nucleotides may be involved in the biochemical mechanisms underlying longer lasting
therapeutic effects associated with ECT, and suggest that peripheral markers can possibly contribute to the evaluation of activity in the central nervous system.