Major depression is a severe and life-threatening illness which represents one of the most important causes of disability world-wide. In particular, about 50% of the affected patients experience a chronic course and up to 20% of them shows an insufficient response to drug treatments (Fava et al., 2003 and Hussain and Cochrane, 2004). As other chronic diseases, major depression is a complex disorder caused by the interaction between environmental and biological/genetic risk factors. Although the molecular alterations underlying the pathogenesis remains to be clearly established, recent preclinical and clinical studies have suggested an involvement of the neurotrophin Brain Derived Neurotrophic Factor (BDNF) in the aetiology of major depression as well as in the antidepressant drug treatment (Angelucci et al., 2005, Castren, 2004, Duman, 2004 and Hashimoto et al., 2004). BDNF is a neurotrophic factor widely expressed in the Central Nervous System (CNS) that plays a major role in brain development, survival and maintenance of neuronal functions and synaptic plasticity. Studies of brain imaging suggest that depressed patients have neuronal atrophy and cell loss in discrete brain regions (Bremner et al., 2000, Krishnan et al., 1993, Kumar et al., 1998, Kumar et al., 2000, Kumar et al., 2004 and Sheline et al., 1996), which are suggestive of a reduction in neuron plasticity. In line with these observations, different studies reported a reduction of BDNF expression in post-mortem brain of depressed subjects (Dwivedi et al., 2001, Dwivedi et al., 2003 and Molnar et al., 2003). Extensive research in rodents has shown that stress-related behaviours can alter the expression of BDNF in the limbic system and cortex (Roceri et al., 2002, Roceri et al., 2004, Smith and Cizza, 1996 and Vollmayr et al., 2001). Furthermore, antidepressant drug treatment enhances BDNF expression and production (Altar, 1999, Castren, 2004, Duman et al., 1997 and Nibuya et al., 1995) and the neurotrophin signalling appears to be required for antidepressant activity in animal models of depression (Castren, 2004, Saarelainen et al., 2003 and Sairanen et al., 2005). The involvement of BNDF in major depression and antidepressant treatment has gained further support from a series of biochemical studies in humans. A decrease in BDNF serum levels has been associated with major depression (Karege et al., 2002a), an effect that is normalized by antidepressant drug therapies (Aydemir et al., 2005 and Shimizu et al., 2003). Moreover a significant correlation between BDNF serum levels and depressive personality traits in a healthy subject was also found (Lang et al., 2004).
Electroconvulsive Therapy (ECT) is one of the eligible therapies for the treatment of major depression (American Psychiatry Association, 2000 and UK ECT Review Group, 2003). Preclinical studies have shown that electroconvulsive seizures (ECS) produces a robust increase in BDNF mRNA (Altar et al., 2004, Chen et al., 2001, Duman et al., 1997, Nibuya et al., 1995 and Zetterstrom et al., 1997) and BDNF protein (Altar et al., 2003) in different rat brain areas. However, whether or not ECT could affect the peripheral levels of BDNF in depressed patients is still an open question. In order to address this issue, we investigated, in the present study, serum levels of BDNF in a group of drug resistant depressed patients before and after ECT.
