A psychobiological model of the etiopathology of major depression is proposed. It is hypothesized that a hyperintentional personality structure, if faced with non-feasible intentional programs in the environment, suffers from inner and outer stress. This stress situation leads to an excess of astrocytic receptors in glial-neuronal synaptic units, called tripartite synapses, and an overexpression of gap junctions in astroglial networks. The imbalance of synaptic information processing caused by the excess of astrocytic receptors leads to a protracted information processing which affects the behavior generating systems in the reticular formation in the brainstem. Since the activation of these systems is delayed, they cannot decide in real time which mode of behavior (e.g. eating, working, communicating, etc.) is appropriate to a specific sensory information from the environment. The modes of behavior comprise all psychobiological action patterns occurring in circadian time periods. A delay of synaptic activation of the systems in the brainstem reticular formation may lead to a displacement of the modes of behavior in the sense of a persistence of some modes (“must do”) and the inability to produce others (”cannot do”). Such a severe behavioral disorder also affects the self-understanding of the patient resulting in a depressive mood. The mechanism of the displacement of the modes of behavior is shown in a computer simulation. Preliminary clinical data may support the model proposed and is briefly discussed.
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