“Too Soon on Earth”: A Biophilosophical Model of Schizophrenia. Some Implications for Humanoid Robots

This paper presents a new explanatory model for schizophrenia based upon philosophical, molecular and neurobiological hypotheses as well as on years of experience in observing and treating these patients. To start with, a novel interpretation of the Hegelian concept of mediation is presented. Mediation is defined as the rejection of non-realizable programs, such as thoughts and ideas, at a certain point in time in the evolution of a living system. Whenever a system treats non-realizable programs as if they were realizable, its ability to “test the reality” is lost, and consequently a loss of ego-boundaries may occur. On the molecular level, I will try to show how “non-splicing” of introns during the mRNA splicing process is equivalent to a loss of the rejection function corresponding to mediation. At the cellular level in the brain, mediation can be explained in terms of glial-neuronal interactions. Glia exert a spatio-temporal boundary setting function determining the grouping of neurons into functional units. Mutations in genes that result in non-splicing of introns can produce truncated (“chimeric”) neurotransmitter receptors. I propose that such dysfunctional receptors are generated in glial cells and that they cannot interact properly with their cognate neurotransmitters. The glia will then lose their inhibitory-rejecting function with respect to the information processing within neuronal networks. This loss of glial boundary setting could be an explanation for the loss of ego or body boundaries in schizophrenia. Pertinent examples of case studies are given attempting to deduce the main symptoms of schizophrenia from the proposed hypothesis. Some implications for the design of delusional robots are also discussed. Finally, the evolutionary potency of non-coding introns is philosophically interpreted that schizophrenics may be “too soon on earth”.

Self-Structuring of Motile Astrocytic Processes within the Network of a Single Astrocyte

Dynamic structuring and functions of perisynaptic astrocytic processes and of the gap junction network within a single astrocyte are outlined. Motile perisynaptic astrocytic processes are generating microdomains. By contacting and retracting of their endfeet an appropriate receptor pattern is selected that modulates the astrocytic receptor sheath for its activation by neurotransmitter substances, ions, transporters, etc. This synaptic information processing occurs in three distinct time scales of milliseconds to seconds, seconds to minutes, hours or longer. Simultaneously, the interconnecting gap junctions are activated by building a network within the astrocyte. Frequently activated gap junction cycles become embodied in gap junction plaques. The gap junction network formation and gap junction plaques are governed and controlled in the same time scales as synaptic information processing. Biomimetic computer systems may represent an alternative to limitations of brainphysiological research. The model proposed allows the interpretation of affective psychoses and schizophrenia as time disorders basically determined by a shortened, prolonged or lacking time scale of synaptic information processing.

The Astrocyte as a Mediator for Self-Reflexive Agents

A model of synapse-astrocyte interactions is proposed which enables repeated neuron-to-neuron connections from the single synapse to the network level. Specifically, the possibility that astrocytes may be organized in networks and processes of a single astrocyte may enable intracellular signaling loops via gap junctions is suggested as a plausible biophysical correlate for hierarchical signaling organization of cyclic pathways. This process ultimately translates to abstract planning, intention and execution of complex actions. The formalism applied is called proemial counting and it enables the generation of cycles of various length in the astroglial network, interpreted as intended action programs. Furthermore, the implementation of a model of the reticular formation in a robot brain based on glial-neuronal interactions is suggested. Finally, the implementation of robot brains with self-reflexive capabilities is discussed.

Astrocyte-Synapse Receptor Coupling in Tripartite Synapses: A Mechanism for Self-Observing Robots

A model of an intentional self-observing system is proposed based on the structure and functions of astrocyte-synapse interactions in tripartite synapses. Astrocyte-synapse interactions are cyclically organized and operate via feedforward and feedback mechanisms, formally described by proemial counting. Synaptic, extrasynaptic and astrocyte receptors are interpreted as places with the same or different quality of information processing described by the combinatorics of tritograms. It is hypothesized that receptors on the astrocytic membrane may embody intentional programs that select corresponding synaptic and extrasynaptic receptors for the formation of receptor-receptor complexes. Basically, the act of self-observation is generated if the actual environmental information is appropriate to the intended observation processed by receptor-receptor complexes. This mechanism is implemented for a robot brain enabling the robot to experience environmental information as “its own”. It is suggested that this mechanism enables the robot to generate matches and mismatches between intended observations and the observations in the environment, based on the cyclic organization of the mechanism. In exploring an unknown environment the robot may stepwise construct an observation space, stored in memory, commanded and controlled by the intentional self-observing system. Finally, the role of self-observation in machine consciousness is shortly discussed.

Psychobiological Model of Volition— Implications for Mental Disorders

A new psychobiological model of volitive processes and its implications for the etiopathology of mental disorders is proposed. The model is based on five elementary volitive processes. These are the volition to act;the volition to self-instrumentalize;the volition to program intentions, the volition to generate realities;and the volition to permanent existence. Imbalances in information processing in tripartite synapses and their network may be responsible for dysfunctions of self-instrumentalization. It is suggested that the volition to permanent existence unconsciously works in mental disorders, but the volition to intentional programming of realities and the volition to generate realities by communication with subjects and objects in their environment are impaired. In depression, the volition to act is constrained by hyperintentional programs that are non-feasible in the environment. In mania volitive processes are totally oriented on events in the environment without any goal-directed pro-gramming. Dysfunctions of volitive processes in schizophrenia are fun-damentally caused by severe impairments of self-instrumentalization. As shown in tripartite synapses a gap between sensory information pro-cessing in the neuronal network and the inner glial networks causes the inability of schizophrenics to distinguish between the self and the other. In delusions, the destiny for communication becomes staged as pseu-do-communication. Together, the study outlines a new model of volitive processes and deduces dysfunctions responsible for communication pa-thology and abnormal reality experiences of patients with mental disor-ders.

Method and Apparatus for Creating Problem-Solving Complexes from Individual Elements

Based on the biological key-lock-principle common in various biological systems such as the human brain, this paper relates to a method and device for creating problem-solving complexes from individual elements that can be coupled with one another and that have different properties to solve problems. The problem solution can be carried out either serially with a large computer, or with several independent, hierarchically joined computers. In this system, an independent control unit that assumes a multitude of tasks and also acts as an interface with access to all participating computers, is assigned to each problem or object class according to the amount of potential problem-oriented solutions. Such a unit prepares the partial solutions found in its computer for the totality of the solutions computed in the associated computers, finally leading to a total problem solution.

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.

Novel Treatment Approach in Schizophrenia: Substitution of Glial Binding Proteins

In chronic schizophrenia, synaptic information processing is unbalanced, as shown in a model of glial-neuronal synaptic units, called tripartite synapses. The glial component of the synapse exerts a modifying function in neurotransmission since the astrocyte activated by neurotransmitters produces gliotransmitters that negatively feedback to the presynapse. It is hypothesized that in schizophrenia nonfunctional astrocytic receptors cannot be activated, thus losing their modulating function. This causes a generalization of information processing in the neuronal networks such that the brain is unable to distinguish between subjects and objects in the environment. Delusions, hallucinations and cognitive impairment occur on the behavioral level. In a model of a cholinergic tripartite synapse, it is shown that glial binding proteins modify neurotransmission by occupancy with cognate neurotransmitters temporarily turning off neurotransmission on the presynapse. Most recently, glial binding proteins have been engineered. It is proposed that the substitution of glial binding proteins may balance synaptic information processing in schizophrenia since these proteins exert a modulatory function comparable to functional astrocytic receptors. Rap- id technical developments may enable this novel treatment approach in schizophrenia.

Insatiable Narcissism Underlying Addictive Behavior: Outline of a Biosystematic Model

This study is a contribution to basic research on narcissism shown on addictive behavior. A new biosystematic model of narcissism underlying addictive behavior is outlined. Basically, normal narcissism is defined as the self-reference of living systems maintaining their circular organization and identity. The communication between narcissistic systems follows the narcissistic logic of fitting or non-fitting of structures (a third possibility is excluded) shown on geometric diagrams. From this model of narcissistic interactions with the environment, addictive behavior is deduced. If the narcissistic desire for the ideal objects cannot be satisfied in the environment, the narcissist attempts to cope with this lack of intended objects by abuse of addictive substances. This leads to an overexpression of receptors in pertinent brain areas that may underly craving on the behavioral level, interpreted as pseudo satisfaction of narcissistic desires—destiny becomes an addiction. In conclusion, the significance of the biosystematic model of narcissism for the understanding of addictive communication and the psychopathology of depression is briefly discussed.