RESUMEN
Frontal asymmetric activation has been proposed to be the underlying mechanism for depression. Some case studies have reported that the enhancement of a relative right frontal alpha activity by an asymmetry neurofeedback training leads to improvement in depressive symptoms. In the present study, we examined whether a neurofeedback training designed to increase the relative activity of the right frontal alpha band would have an impact on symptoms of depressive subjects suffering from emotional, behavioral, and cognitive problems. Our results indicated that the asymmetry neurofeedback training increased the relative right frontal alpha power, and it remained effective even after the end of the total training sessions. In contrast to the training group, the placebo control group did not show a difference. The neurofeedback training had profound effects on emotion and cognition. First, we replicated earlier findings that enhancing the left frontal activity led to alleviation of depressive symptoms. Moreover, cognitive tests revealed that the asymmetry training improved performance of executive function tests, whereas the placebo treatment did not show improvement. We preliminarily concluded that the asymmetry training is important for controlling and regulating emotion, and it may facilitate the left frontal lobe function.
Asunto(s)
Trastorno Depresivo/terapia , Neurorretroalimentación/métodos , Adulto , Ondas Encefálicas/fisiología , Cognición/fisiología , Trastorno Depresivo/fisiopatología , Femenino , Lóbulo Frontal/fisiopatología , Lateralidad Funcional/fisiología , Humanos , Masculino , Proyectos Piloto , Psicoterapia/métodosRESUMEN
Despite its therapeutic success in treating mood-related disorders, little is known about the mechanism by which repetitive transcranial magnetic stimulation (rTMS) alters physiological responses of neurons. Using the forced swim test (FST) in rats as a model of depression, we tested the protective effect of rTMS on synaptic plasticity, specifically, on the induction of hippocampal long-term potentiation (LTP). Male Sprague-Dawley rats were subjected to FST to induce immobility, a behavioral symptom of depression. They were subsequently treated with one of the three conditions: rTMS (rTMS: 1000 stimuli at 10Hz), sham rTMS (SHAM: acoustic stimulation only), or an antidepressant drug, fluoxetine (FLX: 10mg/kg, i.p.) for 7 days. There was a significant difference in immobility time between rTMS and SHAM groups after 7 days of treatment, but not after a single day. Following the second swim test on day 7, they were anesthetized and LTP was induced in vivo in the perforant path-dentate gyrus synapses. Another group (NAIVE) that had received no prior treatment was used as a control for LTP. The SHAM or FLX group exhibited little signs of LTP induction. On the contrary, the rTMS and NAIVE group showed a significant increase in field excitatory postsynaptic potentials after LTP induction. These results show that rTMS has an antidepressant-like effect after a relatively short period of treatment, and this effect might be mediated by a cellular process that can potentially reverse the impaired synaptic efficacy caused by the forced swim procedure.