Abstract
A psychobiological model of the etiopathology of bipolar disorder is proposed. Based on genetic-epigenetic and chronobiological factors 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 imbalances in information processing in glial-neuronal synaptic units, called tripartite synapses. In depression the overexpression of astrocytic receptors and of gap junctions in the astroglial network causes a prolonged information processing which affects the behavior generating systems in the brainstem reticular formation. Because the activation of the behavior generating systems is protracted, they are unable to select an appropriate mode of behavior (e.g. communicating, eating, working, sleeping, etc.) from sensory information in real time. Inversely, in mania astrocytic receptors and gap junctions are underexpressed causing a shortened synaptic information processing with rapid changes in behavior. Switching may represent a coping-attempt with depression by mania and vice versa. Towards a comprehensive model of the pathophysiology of bipolar disorder the role of microglia and their devastating effects on glial-neuronal interactions are outlined. Finally, the testing of the model is discussed.
Highlights
The present study focuses on the central role of astrocytes and their networks in synaptic imbalances, a comprehensive model of pathophysiology of bipolar disorder must refer to microglia and oligodendroglia
If we assume that astrocytic receptors are down-regulated in a manic state leading to excessive dopaminergic activity in synaptic information processing, which subsequently triggers the upregulation of astrocytic receptors, a relative lack of dopamine in the synaptic cleft causes a prolonged information processing
The significance of the present model lies in presenting a new psychobiological model of bipolar disorder based on synaptic imbalances of glia-neuronal interactions which are determined by a hyperintentional personality structure
Summary
Bipolar disorder represents a special syndrome consisting of states of depression or mania with polar-opposite syndromes. Periods between these extreme states represent euthymic states. Most hypothetical models of depression and bipolar disorder are neurocentric, experimental findings indicate that the glial system, especially astrocytes and microglia, plays a significant role in the pathophysiology of affective disorders [9] [10] [11]. The pathophysiological model of bipolar disorder here proposed is based on glial-neuronal interactions focusing on imbalances in astrocyte-neuronal synaptic units, called tripartite synapses [14] [15] [16] [17]
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