Model of the Reticular Formation of the Brainstem Based on Glial-Neuronal Interactions.

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.

Balancing and imbalancing effects of astrocytic receptors in tripartite synapses. Common pathophysiological model of mental disorders and epilepsy.

Based on a logic of balance mechanisms influencing information processing in tripartite synapses are proposed. It is hypothesized that the number of expressed astrocytic receptors determines balanced and imbalanced synaptic states. Synaptic information processing in mental disorders is underbalanced in depression, overbalanced in mania, and completely unbalanced in schizophrenia.

Intuition in autistic savantism: a hypothetical model based on glial-neuronal interactions.

The previously proposed hypothesis on the astrocyte mega-domains of autistic savantism is here further elaborated with regard to the faculty of intuition. Two mechanisms may essentially be responsible for the intuition of autistic savantism. First, the increased number of contacted synapses via the astrocyte processes enables the brain to generate a comprehensive perception of a scene in the environment.

Confidence analyses of self-interpretation and self-description in depressive behaviour.

The present paper represents an investigation in the procedure to validate a new questionnaire (Salzburg Subjective Behavioural Analysis, SSBA). This questionnaire is based on a new approach to the diagnosis of depressive behaviour. It is hypothesized that a patient suffering from a depressive disorder loses the ability to produce one or more modes of behaviour at a given time and simultaneously has the urge to produce one or more modes of behaviour constantly.

Neuromodulatory systems.

We examine the interactions and interdependencies between Neuroglia, the Brain-Cell Microenvironment, and the processes commonly subsumed under Neuromodulation. The interactions of the component processes covering a wide spectrum of frequencies are designated as Neuromodulatory Systems (NMS). This implies NMS's scale-invariance as the capacity of linking actions across many time scales, and self-similarity at any scale.

Astrocyte mega-domain hypothesis of the autistic savantism.

Individuals with autism who show high abilities are called savants. Whereas in their brains a disconnection in and between neural networks has been identified, savantism is yet poorly understood. Focusing on astrocyte domain organization, it is hypothesized that local astrocyte mega-organizations may be responsible for exerting high capabilities in brains of autistic savants.

[Dissociation (conversion) - malingering - antisocial personality disorder: differential diagnostic reflection on the basis of a case study].

In this case report we refer to the big challenge of making a diagnosis in a deliberate malingering in the field of mental disorders. We specifically describe the difficulty regarding the differentiation between a conversion disorder and malingering of a serial delinquent. For such a person avoiding criminal persecution is one of the most frequent reason to deceitfully simulate a mental illness.

Possible role of glia in cognitive impairment in schizophrenia.

Cognitive impairment is a core disorder of the schizophrenia syndrome. Based on glial-neuronal interactions, a pathophysiological model is proposed that could be explanatory for cognitive impairment in schizophrenia. The model consists of three main hypotheses concerning the pathophysiology in tripartite synapses, oligodendrocyte-axonic interactions, and in the glial networks (astrocytic syncytium).

Possible effects of synaptic imbalances on oligodendrocyte-axonic interactions in schizophrenia: a hypothetical model.

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.

Comprehensive behavioral analysis of patients with a major depressive episode.

Background: A major depressive episode diagnosed according to DSM-IV criteria can be accompanied by symptoms that DSM-IV does not include. These symptoms are sometimes classified as comorbidities. Our study assessed altered behavioral modes during a major depressive episode; ie, if 1 or more modes of behavior operated less or even not at all ("never"), or if the operation of others was more frequent or even constant ("always").

The gliocentric hypothesis of the pathophysiology of the sudden infant death syndrome (SIDS).

The hypothesis is based on glial-neuronal interactions in the cardio-respiratory centre of the brainstem. Recently, it has been experimentally verified that glial cells, especially astrocytes, exert a modulatory function in the maintenance of homeostasis in this brain region. In addition, astrocytes may also control the rhythms of heartbeat and breathing in a pulsatile manner.

[Method and empirical results from expert opinions on 90 offenders concerning the question of complete intoxication].

Based on a 3-year sample of expert opinions concerning the question of complete intoxication (n = 90), methodology and results are presented. Since more than half of the offenders (n = 53) claim amnesia regarding the circumstances of the offence, this subjective amnesia is considered methodologically. If the file contains observations on the offender's behaviour, it is generally possible to assess if the offender was still able to self-reflect and act in a purposeful way.

Downregulation and upregulation of glial connexins may cause synaptic imbalances responsible for the pathophysiology of bipolar disorder.

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.

Synaptic imbalances in endogenous psychoses.

Based on the formalism of logical balance, imbalances of information processing in tripartite synapses are described as a possible explanation for the pathophysiology of endogenous psychoses like depression, mania and schizophrenia. A tripartite synapse consists of the presynapse, the synaptic cleft, the postsynapse (neuronal components) and the glia (glial components). According to the logic of balance in a living system, the number of values and the number of variables must be equal.

The syncytiopathy hypothesis of depression: downregulation of glial connexins may protract synaptic information processing and cause memory impairment.

Astrocytes interconnected via gap junctions build an astrocytic syncytium. Gap junctions are composed of connexin proteins that are activated by substances of the neuronal system. It is hypothesized that disorders in the astrocytic syncytium may represent a main component of the pathophysiology of depression, called syncytiopathy.

Loss of function of glial gap junctions may cause severe cognitive impairments in schizophrenia.

A generalized cognitive deficit is at the core of schizophrenia. It is hypothesized that a loss of function of glial gap junctions may cause severe cognitive impairment in schizophrenia. Glial gap junctions are electrical channels that may register the neuronal activation frequencies of glial-neuronal compartments by generating gap junction plaques.

Loss of self-understanding: a behavior-oriented model of depression.

Background: A new model of depression is proposed which is biological and explanatory on the behavioral level. It is hypothesized that a patient suffering from a depressive disorder loses the ability to produce one or more modes of behavior at a given time and simultaneously has the urge to produce one or more other modes of behavior constantly. The patient is also unable to interpret his behavioral disorder ("loss of self-understanding").

The incoherence hypothesis of schizophrenia: based on decomposed oligodendrocyte-axonic relations.

Based on the findings of white matter abnormalities in brains with schizophrenia, it is hypothesized that this disorder may be responsible for symptoms of incoherence of schizophrenia. It is supposed that the processes of oligodendrocytes tie the various properties of axonic information conductance together into categories. For this oligodendrocytic computation capacity a formalism is proposed.

Nonfunctional glial proteins in tripartite synapses: a pathophysiological model of schizophrenia.

A model for the pathophysiology of schizophrenia is proposed that focuses on an unbalance of transmission in tripartite synapses. Synaptically associated astrocytes should be viewed as integral modulatory elements of tripartite synapses consisting of the presynapse, the postsynapse, and the glial element. Astrocytes may secrete glial binding protein into the synaptic cleft, thus binding free neurotransmitters and thereby reducing the levels of neurotransmitters available for stimulating the postsynapse.

Imbalance of glial-neuronal interaction in synapses: a possible mechanism of the pathophysiology of bipolar disorder.

There is a wave of new information suggesting that glia, especially astrocytes, are intimately involved in the active control of neuronal activity and synaptic transmission. Synaptically associated astrocytes should be viewed as integral modulatory elements of tripartite synapses consisting of the presynapse, the postsynapse, and the glial element (astrocytes). Smit and coworkers proposed a model of a cholinergic tripartite synapse based on the identification of a glial-derived binding protein (BP) that is secreted into the synapse and binds free acetylcholine (ACh), thus reducing the levels of ACh available for stimulating the postsynapse.

The self-composing brain: towards a glial-neuronal brain theory.

A brain model is proposed which describes its structural organization and the related functions as compartments organized in time and space. On a molecular level the negative feedback loops of clock-controlled genes are interpreted as compartments. This spatio-temporal operational principle may also work on the cellular level as glial-neuronal interactions, wherein glia have a spatio-temporal boundary setting function.