Psychobiological model of major depressive disorder

Abstract

A novel psychobiological model of major depression based on glial-neuronal interactions is proposed. Imbalance of information processing in tripartite synapses and the astroglial networks may be essentially caused by overexpression of astrocytic receptors and gap junctions in the astroglial network. Basic genetic and epigenetic predisposition as well as internal and/or external stress may be responsible for this dysregulation of information processing in depression. Both personality structure and the excess of astrocytic receptors and astroglia gap junctions cause a relative lack of neurotransmitter substances with protracted information processing. Since it has been hypothesized that intentional programs are generated in the astroglial network, the brain operates hyperintentionally in depression. Increased coupling of gap junctions leads to an expansion of the astroglial domain organization such that the astrocytic domains overlap with cognitive impairment as a consequence. The basic symptoms of depression can be deduced from the proposed model. Finally, an action oriented treatment based on antidepressant therapy is outlined.

Keywords: major depression, synaptic imbalance, astrocytic receptors, glial connexins, overexpression, treatment