Abstract
With more than 350 million depressed individuals worldwide, major depressive disorder is one of the most common psychiatric illnesses. Although, the pathophysiology of depression is far from being fully understood, five decades of development of different classes of antidepressants targeting central monoaminergic systems (serotonin, noradrenaline and dopamine) has led to the emergence of the monoaminergic hypothesis. However, despite a growing number of available pharmacotherapies, treatment of major depression nevertheless remains unsatisfactory.
Highlights
Ten years ago it was postulated that abnormal functioning of glial cells, of astrocytes, contribute to the physiopathology of depression
We showed that acute deep brain stimulation (DBS) induced a rapid increase of hippocampal neurogenesis, reversed the effects of stress on hippocampal synaptic metaplasticity, increased spontaneous infralimbic part of the prefrontal cortex (IL-PFC) low-frequency oscillations and both raphe 5-HT firing activity and synaptogenesis
Recent studies aimed to characterize the role played by A1 receptors in the shape of action potentials and the regulation of axonal conductance report that the administration of an adenosine antagonist increases the width of axonal action potentials. This result suggests that astrocytes, through the release of adenosine and subsequent A1 receptor stimulation, space (Kofuji and Newman, 2004), we hypothesized that an alteration of astrocyte function within the lesioned site leads to an accumulation of extracellular K+ which, in turn, would produce a depolarization of neuron membrane and a blockade of DBS-mediated effects
Summary
Ten years ago it was postulated that abnormal functioning of glial cells, of astrocytes, contribute to the physiopathology of depression (for review, Rajkowska and Miguel-Hidalgo, 2007). Bekar et al (2008) have shown in vitro that DBS was associated with an increase of ATP outflow within the thalamus, resulting in an accumulation of adenosine, which in turn depressed excitatory transmission through A1 receptors activation.
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