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Mitterauer B.J.,Volitronics Institute for Basic Research | Kofler-Westergren B.,University of Salzburg
Frontiers in Psychiatry | Year: 2011

A model of glial-neuronal interactions is proposed that could be explanatory for the demyelination identified in brains with schizophrenia. It is based on two hypotheses: (1) that glia-neuron systems are functionally viable and important for normal brain function, and (2) that disruption of this postulated function disturbs the glial categorization function, as shown by formal analysis. According to this model, in schizophrenia receptors on astrocytes in glial-neuronal synaptic units are not functional, loosing their modulatory influence on synaptic neurotransmission. Hence, an unconstrained neurotransmission flux occurs that hyperactivates the axon and floods the cognate receptors of neurotransmitters on oligodendrocytes. The excess of neurotransmitters may have a toxic effect on oligodendrocytes and myelin, causing demyelination. In parallel, an increasing impairment of axons may disconnect neuronal networks. It is formally shown how oligodendrocytes normally categorize axonic information processing via their processes. Demyelination decomposes the oligodendrocyte-axonic system making it incapable to generate categories of information. This incoherence may be responsible for symptoms of disorganization in schizophrenia, such as thought disorder, inappropriate affect and incommunicable motor behavior. In parallel, the loss of oligodendrocytes affects gap junctions in the panglial syncytium, presumably responsible for memory impairment in schizophrenia. © 2011 Mitterauer and Kofler-Westergren. Source

Mitterauer B.J.,Volitronics Institute for Basic Research
CNS Neuroscience and Therapeutics | Year: 2011

The model of the pathophysiology of bipolar disorder proposed is based on imbalances in tripartite synapses caused by dysregulations of connexin expression in the astrocytic syncytium. If the expression of connexins is downregulated, a compensatory upregulation of astrocytic receptors may occur and be responsible for the pathophysiology of depression. Conversely, if the expression of connexins is upregulated, the expression of the astrocytic receptors may be downregulated and be responsible for the pathophysiology of mania. In depression, a relative lack of neurotransmitters exerts a protracted synaptic information processing, whereas in mania a relative increase of neurotransmitters may accelerate synaptic information processing. In addition, the modulatory role of gliotransmitters may be affected in bipolar disorder. Since the dysregulations of connexins impair the astrocytic syncytium, these disorders could be explanatory for cognitive impairment both in depression and in mania. Finally, the testability of this model is discussed. © 2010 Blackwell Publishing Ltd. Source

Mitterauer B.J.,Volitronics Institute for Basic Research
Journal of Intelligent Systems | Year: 2010

The cellular structure of the brain consists of the neuronal system and the glial system. Therefore, a pure neurophilosophy is based on an ontological fault. Here, a brain model is proposed referring to both cell systems. The organization of glial-neuronal interactions in domains is interpreted as a polyontological structure in the sense of many ontological loci or subjective realities. The ontological loci can cooperate (polycontexturality) or gaps exist between them (discontexturality). For the formal description of the polyontological structure of the brain morphogrammatics is applied. Moreover, the holistic and integrative function of selfreference guarantees the maintenance of the circular organization of the brain implying the time conception of permanence. Glial-neuronal synaptic units are interpreted as consciousness generating units, called proemial synapses. It is hypothesized that the intentional programming of these synapses occurs in the glial networks (syncytia). Since the testability of my brain model with biological methods is limited, the construction of a robot brain may be promising. Finally, the issue of dualism in current neurophilosophy is discussed. Source

Mitterauer B.J.,Volitronics Institute for Basic Research
International Journal of Machine Consciousness | Year: 2013

The paper starts out with a discussion of the difference between mythology and feasible concepts in robotics. Based on a novel brain model and an appropriate formalism, a distinction is made between auto-reflection and hetero-reflection of the robot and self-reflection of its constructor. Whereas conscious robots are able to auto-reflect their mechanical behavior and hetero-reflect the behavior with regard to the environment, the capability of self-reflection must remain within the constructor of the robot. This limitation of the construction of conscious robots is mainly brain-theoretically and philosophically founded. Finally, it is proposed that in addition to a second nature, human technology may succeed in creating a third nature embodied as a society of robots. © 2013 World Scientific Publishing Company. Source

Mitterauer B.J.,Volitronics Institute for Basic Research
Cognitive Computation | Year: 2014

A new model of the reticular formation of the brainstem is proposed. It refers to the neuronal and glial cell systems. Thus, it is biomimetically founded. The reticular formation generates modes of behavior (sleeping, eating, etc.) and commands all behavior according to the most appropriate environmental information. The reticular formation works on an abductive logic and is dominated by a redundancy of potential command. Formally, a special mode of behavior is represented by a comprehensive cycle (Hamilton loop) located in the glial network (syncytium) and embodied in gap junctional plaques. Whereas for the neuronal network of the reticular formation, a computer simulation has already been presented; here, the necessary devices for computation in the whole network are outlined. © 2014, The Author(s). Source

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