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.

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.

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.

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.

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.