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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

Schematic diagram of the glial–neuronal interaction. Two astrocytes (Ac1, 2) are shown in this very simple model, whereby in each case only one neuron belonging to an astrocyte is taken into consideration. The glial network (syncytium) consists of two astrocytes and two oligodendrocytes (Oc1, 2) belonging to them. Gap junctions (g.j.) exist between the astrocytes and the oligodendrocytes. The neuronal system shows two neurons (N1, 2) with two afferent axons (Axi, j) and two afferent axodendritic synapses (Sai, j), two efferent axons (Ax1, 2) with myelin sheaths (Ms) and a node of Ranvier (N.R.), as well as two dendro-dendritic synapses (Sd1,2,3,4) with the corresponding dendrites (D1, D2, D3, D4).
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Figure 1: Schematic diagram of the glial–neuronal interaction. Two astrocytes (Ac1, 2) are shown in this very simple model, whereby in each case only one neuron belonging to an astrocyte is taken into consideration. The glial network (syncytium) consists of two astrocytes and two oligodendrocytes (Oc1, 2) belonging to them. Gap junctions (g.j.) exist between the astrocytes and the oligodendrocytes. The neuronal system shows two neurons (N1, 2) with two afferent axons (Axi, j) and two afferent axodendritic synapses (Sai, j), two efferent axons (Ax1, 2) with myelin sheaths (Ms) and a node of Ranvier (N.R.), as well as two dendro-dendritic synapses (Sd1,2,3,4) with the corresponding dendrites (D1, D2, D3, D4).

Mentions: The proposed biological brain model is based on glial–neuronal interactions (Mitterauer, 1998, 2007). The nervous tissue of the brain consists of the neuronal system (neurons, axons, dendrites) and the glial system (astrocytes, oligodendrocytes with myelin sheaths enfolding axons, radial glia, and microglia). Experimental results are inspiring a major reexamination of the role of glia in the regulation of neural integration in the central nervous system (Kettenmann and Ransom, 2005; Halassa and Haydon, 2010). Figure 1 shows a schematic diagram of the glial–neuronal interaction: two astrocytes (Ac1,2) are shown in this very simple model, whereby in each case only one neuron (N1,2) belonging to an astrocyte is taken into consideration. Halassa et al. (2007) identified how a single astrocyte contacts only four to eight neurons, but 300–600 synapses via its processes. The glial network (syncytium) consists in this schema of two astrocytes and two oligodendrocytes (Oc1,2) interconnected via gap junctions (g.j.). The neuronal system shows two neurons (N1,2) with two afferent axons (Axi,j) and two afferent axodendritic synapses (Sai,j), two efferent axons (Ax1,2) with myelin sheaths (Ms) and a node of Ranvier (N.R.), as well as two dendro-dendritic synapses (Sd1,2,3,4) with the corresponding dendrites (D1,D2;D3D4).


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

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

Schematic diagram of the glial–neuronal interaction. Two astrocytes (Ac1, 2) are shown in this very simple model, whereby in each case only one neuron belonging to an astrocyte is taken into consideration. The glial network (syncytium) consists of two astrocytes and two oligodendrocytes (Oc1, 2) belonging to them. Gap junctions (g.j.) exist between the astrocytes and the oligodendrocytes. The neuronal system shows two neurons (N1, 2) with two afferent axons (Axi, j) and two afferent axodendritic synapses (Sai, j), two efferent axons (Ax1, 2) with myelin sheaths (Ms) and a node of Ranvier (N.R.), as well as two dendro-dendritic synapses (Sd1,2,3,4) with the corresponding dendrites (D1, D2, D3, D4).
© Copyright Policy - open-access
Related In: Results  -  Collection

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

Figure 1: Schematic diagram of the glial–neuronal interaction. Two astrocytes (Ac1, 2) are shown in this very simple model, whereby in each case only one neuron belonging to an astrocyte is taken into consideration. The glial network (syncytium) consists of two astrocytes and two oligodendrocytes (Oc1, 2) belonging to them. Gap junctions (g.j.) exist between the astrocytes and the oligodendrocytes. The neuronal system shows two neurons (N1, 2) with two afferent axons (Axi, j) and two afferent axodendritic synapses (Sai, j), two efferent axons (Ax1, 2) with myelin sheaths (Ms) and a node of Ranvier (N.R.), as well as two dendro-dendritic synapses (Sd1,2,3,4) with the corresponding dendrites (D1, D2, D3, D4).
Mentions: The proposed biological brain model is based on glial–neuronal interactions (Mitterauer, 1998, 2007). The nervous tissue of the brain consists of the neuronal system (neurons, axons, dendrites) and the glial system (astrocytes, oligodendrocytes with myelin sheaths enfolding axons, radial glia, and microglia). Experimental results are inspiring a major reexamination of the role of glia in the regulation of neural integration in the central nervous system (Kettenmann and Ransom, 2005; Halassa and Haydon, 2010). Figure 1 shows a schematic diagram of the glial–neuronal interaction: two astrocytes (Ac1,2) are shown in this very simple model, whereby in each case only one neuron (N1,2) belonging to an astrocyte is taken into consideration. Halassa et al. (2007) identified how a single astrocyte contacts only four to eight neurons, but 300–600 synapses via its processes. The glial network (syncytium) consists in this schema of two astrocytes and two oligodendrocytes (Oc1,2) interconnected via gap junctions (g.j.). The neuronal system shows two neurons (N1,2) with two afferent axons (Axi,j) and two afferent axodendritic synapses (Sai,j), two efferent axons (Ax1,2) with myelin sheaths (Ms) and a node of Ranvier (N.R.), as well as two dendro-dendritic synapses (Sd1,2,3,4) with the corresponding dendrites (D1,D2;D3D4).

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