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

Mitterauer BJ, Kofler-Westergren B - Front Psychiatry (2011)

Bottom Line: The excess of neurotransmitters may have a toxic effect on oligodendrocytes and myelin, causing demyelination.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.

View Article: PubMed Central - PubMed

Affiliation: Volitronics - Institute for Basic Research, Psychopathology and Brain Philosophy Wals/Salzburg, Austria.

ABSTRACT
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.

No MeSH data available.


Related in: MedlinePlus

Example of an oligodendrocyte-axonic structure according to the rule of categorization (Table 1). Oligodendrocytes (Oc) and myelin sheaths (Ms) are represented in red color. Ten axons (black) with different or equal properties of information processing (1…4) are shown. Each oligodendrocyte is characterized with the category that its processes generate. From the left to the right examples of one to four processes (according to Table 1) are given. Blue colored processes connect axonic property 1, green property 2, yellow property 3, and brown property 4.
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Figure 5: Example of an oligodendrocyte-axonic structure according to the rule of categorization (Table 1). Oligodendrocytes (Oc) and myelin sheaths (Ms) are represented in red color. Ten axons (black) with different or equal properties of information processing (1…4) are shown. Each oligodendrocyte is characterized with the category that its processes generate. From the left to the right examples of one to four processes (according to Table 1) are given. Blue colored processes connect axonic property 1, green property 2, yellow property 3, and brown property 4.

Mentions: Figure 5 gives an example how oligodendrocytes with one to four processes connect 10 axonic lines with four different properties (1…4). Each oligodendrocyte is characterized with the category that its processes generate. From the left to the right examples of one to four processes (according to Table 1) are given. Together, the capacity of the oligodendrocyte–axonic system to generate categories may lead to a coherent information processing. Coherence in cognition means that we are able to abstract, generalize, and extract meaning from different properties of information. This capacity can be severely disturbed in schizophrenia.


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

Mitterauer BJ, Kofler-Westergren B - Front Psychiatry (2011)

Example of an oligodendrocyte-axonic structure according to the rule of categorization (Table 1). Oligodendrocytes (Oc) and myelin sheaths (Ms) are represented in red color. Ten axons (black) with different or equal properties of information processing (1…4) are shown. Each oligodendrocyte is characterized with the category that its processes generate. From the left to the right examples of one to four processes (according to Table 1) are given. Blue colored processes connect axonic property 1, green property 2, yellow property 3, and brown property 4.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC3102422&req=5

Figure 5: Example of an oligodendrocyte-axonic structure according to the rule of categorization (Table 1). Oligodendrocytes (Oc) and myelin sheaths (Ms) are represented in red color. Ten axons (black) with different or equal properties of information processing (1…4) are shown. Each oligodendrocyte is characterized with the category that its processes generate. From the left to the right examples of one to four processes (according to Table 1) are given. Blue colored processes connect axonic property 1, green property 2, yellow property 3, and brown property 4.
Mentions: Figure 5 gives an example how oligodendrocytes with one to four processes connect 10 axonic lines with four different properties (1…4). Each oligodendrocyte is characterized with the category that its processes generate. From the left to the right examples of one to four processes (according to Table 1) are given. Together, the capacity of the oligodendrocyte–axonic system to generate categories may lead to a coherent information processing. Coherence in cognition means that we are able to abstract, generalize, and extract meaning from different properties of information. This capacity can be severely disturbed in schizophrenia.

Bottom Line: The excess of neurotransmitters may have a toxic effect on oligodendrocytes and myelin, causing demyelination.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.

View Article: PubMed Central - PubMed

Affiliation: Volitronics - Institute for Basic Research, Psychopathology and Brain Philosophy Wals/Salzburg, Austria.

ABSTRACT
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.

No MeSH data available.


Related in: MedlinePlus