RESUMEN
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.
Asunto(s)
Plaquetas/metabolismo , Catatonia/terapia , Terapia Electroconvulsiva/métodos , Proteínas de Transporte de Serotonina en la Membrana Plasmática/sangre , Anciano , Catatonia/sangre , Catatonia/complicaciones , Clomipramina/uso terapéutico , Trastorno Depresivo Mayor/sangre , Trastorno Depresivo Mayor/complicaciones , Trastorno Depresivo Mayor/terapia , Relación Dosis-Respuesta a Droga , Femenino , Humanos , Escalas de Valoración Psiquiátrica , Inhibidores Selectivos de la Recaptación de Serotonina/metabolismo , Inhibidores Selectivos de la Recaptación de Serotonina/uso terapéutico , Factores de TiempoRESUMEN
Serotonin transporter (SERT) was studied by [3H]-paroxetine binding in blood platelets from controls and epileptic patients with generalized convulsive seizures. The average KD and BMax were not different in the two cases. However, a significant decrease was found in the serotonin transporter density in the platelet membranes from patients having undergone an epileptic seizure less than 4 days before. This circumstance may indicate a homeostatic reaction to the epileptic attack.
Asunto(s)
Plaquetas/metabolismo , Epilepsia Tónico-Clónica/metabolismo , Glicoproteínas de Membrana/sangre , Proteínas de Transporte de Membrana/sangre , Proteínas del Tejido Nervioso/sangre , Convulsiones/metabolismo , Adulto , Anciano , Anciano de 80 o más Años , Femenino , Humanos , Masculino , Persona de Mediana Edad , Paroxetina/sangre , Paroxetina/farmacocinética , Serotonina/sangre , Proteínas de Transporte de Serotonina en la Membrana Plasmática , Inhibidores Selectivos de la Recaptación de Serotonina/sangre , Inhibidores Selectivos de la Recaptación de Serotonina/farmacocinéticaRESUMEN
The binding of labelled paroxetine to the serotonin transporter (SERT) of platelet membranes has been studied in both venous and mixed venous/arterial blood of the rat. In addition, we studied the inhibition of paroxetine binding to SERT by quipazine and N-methyl-quipazine (NMQ). The results indicate differences in affinity for the two test drugs, quipazine and NMQ, in venous vs. mixed venous/arterial blood. This suggests different post-translational modifications of SERT in platelets of arterial vs. venous blood.