Psychobiological Model of Bipolar Disorder: Based on Imbalances of Glial-Neuronal Information Processing

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.

Pathophysiology of Schizophrenia Based on Impaired Glial-Neuronal Interactions

The model of impaired glial-neuronal interactions in schizophrenia is based on the core hypothesis that non-functional astrocyte receptors may cause an unconstrained synaptic information flux such that glia lose their modulatory function in tripartite synapses. This may lead to a generalization of information processing in the neuronal networks responsible for delusions and hallucinations on the behavioral level. In this acute paranoid stage of schizophrenia, non-functional astrocytic receptors or their loss decompose the astrocyte domain organization with the effect that a gap between the neuronal and the glial networks arises. If the illness progresses the permanent synaptic neurotransmitter flux may additionally impair the oligodendrocyte-axonic interactions, accompanied by a “creeping” decay of oligodendroglia, axons and glial gap junctions responsible for severe cognitive impairment. Here we may deal with after-effects caused by the basic fault of information processing in tripartite synapses. The gaps between the neuronal and glial networks prohibit the neuronal reality testing of intentional programs presumably generated in the glial networks, called schizophrenic dysintentionality. In non-schizophrenic delusions glia may not be disturbed, but exhausted extrasynaptic information processing may cause an unconstrained synaptic flux responsible for delusions.

Computer system for simulation of human perception. Some implications for the pathophysiology of the schizophrenic syndrome

After the description of a brain model based on glial-neuronal interactions, a computer system for simulation of human perception, called clocked perception system, is proposed. The computer system includes a receptor field with sensors, each of which receives data with specific characteristics. These data are passed to processors, whereby only those connections between sensors and processors are released that are suited for an evaluation of the data according to a combination of specific data dictated by a phase program circuit. The computer system also includes a selector circuit that discards those dictated program commands that lead to a “senseless” computation result. A motor program circuit for the control of effectors may be connected to the computer system which at least contributes to the movement of the receptor field in order to bring the receptor field closer to suitable data with specific characteristics for better execution of the program. From disorders of the computer system implications are deduced for the pathophysiology of the schizophrenic syndrome. Finally, a novel treatment approach to this syndrome is proposed.